Scgf gene is usually up-regulated in brain tumors, including supratentorial ependymoma (153), Ewing family tumor (one of small round blue tumor associated with EWS/FLI1 translocation is estimated to be originated in tumorigenesis between neural crest from neural ectoderm and mesenchymal-vascular endothelial lineage) (154,249), radiosensitive glioblastoma (155) and glioma (156). Scgf gene is down-regulated along with differentiation of ST1 glioma cells by treating with glucocorticoid or all trans-retinoic acid (156). Correlated up-regulation of cyclin D1 with scgf in Ewing's sarcoma compared to rhabdomyosarcoma (GSE967 dataset) suggests some functional and etiological roles of scgf in cell cycle (516). There is no significant change between the level of scgf gene expression in glioblastoma multiforme cancer stem cell line and neural stem cell line (237). SCGF production is up-regulated by GL261 glioblastoma multiforme cells surviving after in vitro treatment with doxorubicin or irradiation (487). Scgf gene expression is up-regulated in glioblastoma tissue and serum SCGF level is elevated
in the serum from glioblastoma patients compared to normal controls (514). Plasma SCGF level significantly increases in recurrent glioblastoma patients 28 days after treatment with aflibercept, a recombinant decoy receptor that sequesters both VEGF and PlGF (334). When GD2+ M059K glioblastoma cells are cocultured for 3 days with combination of N-803 (IL-15N72D mutein superagonist coupled with IL-15RαSu/IgG1Fc), anti-GD2 MoAb dinutuximab and ex vivo expanded NK cells, NK cell-mediated cytotoxicity is enhanced against M059K cells to reduce their SCGF secretion (656).
  No unique somatic mutation of scgf gene has been reported in glioma (Wellcome Trust Sanger Institute).        
  Experimental ischemia induces scgf gene up-regulation in the damaged cerebral cortex, indicating that intrinsic neuroprotective strategies are working as seen in hibernation-induced hypoxemia (180).
  Scgf gene down-regulation is demonstrated in neurodegenerative diseases from the controlled studies of one healthy and other morbid Finnish identical twins with multiple sclerosis (181) and waddles mice characterized by carbonic anhydrase VIII deficiency in cerebellar Purkinje cells (54). Serum SCGF level is elevated in the Russian familial hemiplegic migraine patients with cerebellar ataxia and CACNA1A R583Q mutation compared to blood relatives of migraine patients without R583Q mutation (566). SCGF level is significantly lower in the serum from patients with multiple sclerosis at onset than healthy controls (496). Cerebrospinal fluid SCGF level is significantly higher in patients with chronic inflammatory demyelinating polyneuropathy than those with multiple sclerosis or non-inflammatory neurologic disorders (573).
  Plasma SCGF level is significantly higher in patients with silent brain infarcts than those with lacunar infarcts (423).
  There have been some SCGF-related reports of unknown significance in autism spectrum disorder (ASD) (183), SNP ([a/g]rs722036) in schizophrenia (Pat4) and Alzheimer's disease (184). Scgf gene is hypermethylated in the hippocampus from patients with Alzheimer's disease (603). SCGF level in the cerebrospinal fluid correlates with negative cerebral retention of 11C-Pittsburgh compound B and CSF level of all tau and T181-phosphorylated tau protein in patients with mild cognitive impairment (570). Glycosphingolipid-related genes are down-regulated in the Brodmann area 46 of cerebral cortex from the patients with schizophrenia (178). Ingenuity pathway analysis indicates an interaction of those gene up-regulation with scgf gene. A hemizygous 63.8kb deletion of 5' 20-exon of SHANK1 (SH3 and multiple ankyrin repeat domain 1) and neighboring whole scgf genes on chromosome 19q13.33 is identified in a Canadian four-generation family, in which 4 males but not 2 females have high functioning ASD (368). Scgf DNA methylation is negatively correlated in peripheral leukocytes from ASD patients and discordant disease-free sibling pair (687). Plasma SCGF level from male ASD patients is not different from matched controls (338). There is no significant difference in SCGF concentration in the cerebrospinal fluid from patients with neurologic post-treatment Lyme disease and chronic fatigue syndrome, and healthy control subjects (308). No significant change in the plasma SCGF level is observed between elderly patients with depression and normal controls (214).
  Prolonged social isolation in adult rats induces anxiety- and anhedonia-like symptoms and decreased cAMP response element-binding protein (CREB) in the nucleus accumbens shell (NAcSh). Anxiety-, but not anhedonia-like symptoms are reversed by chronic CREB overexpression with adeno-associated virus vector in the NAcSh of socially isolated rats, and scgf gene expression is down-regulated in the CREB-overexpressed NAcSh tissue relative to GFP-expressed control (390).
  Endoplasmic reticulum stress inducer is estimated one of the pathogenesis of cerebral diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, Lou Gehrig's disease or prion disease. Endoplasmic reticulum stress inducer, thapsigargin, inhibits protein synthesis of human astrocytoma cell line, U-87MG; scgf gene is 3-fold down-regulated. P-methoxycinnamic acid ethylester, caffeic acid, 8-O-E-p-methoxycinnamoyl harpagide or Sarophularia ningpoensis protects U-87MG cells from thapsigargin-induced inhibition of protein synthesis, i.e. scgf gene is 1.9-fold up-regulated as compared with the controls treated with thapsigargin alone (202). Scgf gene expression is up-regulated in SNCA triplication-positive neural stem cells differentiated in the dopaminergic culture of iPS cells from patients with Parkinson’s disease (524).
  Scgf gene expression is down-regulated in SH-SY5Y human neuroblastoma cells treated with aluminum-β1-42-amyloid complex but not with aluminum or β1-42-amyloid (307).
  Scgf mRNA, hsa-miR-378c,d,f,i miRNA and ENST00000590159.1 lncRNA are differentially and interrelatedly expressed in human intracranial saccular aneurysm (556).
  SCGF level is significantly elevated in the cerebrospinal fluid from patients with trigeminal neuralgia (675). An SCGF concentration in the cerebrospinal fluid is not different among patients with Guillan-BarrÉ syndrome, chronic inflammatory demyelinating polyneuropathy, diabetic polyneuropathy and headache controls (258). There is no significant difference between serum SCGF level from patients with chronic inflammatory demyelinating polyneuropathy and healthy controls (483). SCGF level in cerebrospinal fluid from a pandemic H1N1 influenza viral infection-associated encephalopathy is lower than those from patients with central nervous system (CNS) infection or viral infection without CNS involvement (313).
  Plasma SCGF level from patients with acute (490) and chronic (424) spinal cord injury is significantly higher than uninjured controls, and increases with the time from initial injury. SCGF level in cerebrospinal fluid is negatively associated with MAS (modified Ashworth scale) of patients with spinal cord injury between admission and discharge (635). SCGF is detected in the conditioned media from rat injured and adjacent rostral but not caudal spinal cord (456). Interlaminar epidural steroid injection significantly ameliorates low back pain and lowers plasma SCGF level 7 to 10 days after the therapy for patients with intervertebral disc disorders, particularly disc herniation (513).
  Scgf gene expression is significantly up-regulated in the translating ribosome affinity purified cholinergic habenular neurons from ChAT-DW167 transgenic mice during withdrawal after chronic nicotine administration (429).
  SCGF level in the serum from patients with mitochondrial diseases is lower than other disease controls (482,

  Retinal degeneration is a hereditary disease with vascular atrophy leading to blindness. When normal hematopoietic stem cells (HSC) are transplanted into the lens of retinal degeneration rd1/rd1SCID mice, scgf gene is up-regulated in the retinal cone as degenerative retinal vessels are recovered with normal HSCs-derived EPCs (63). SCGF level is significantly elevated in the vitreous from patients with proliferative vitreoretinopathy relative to primary retinal detachment (RD) and macular pucker vitreous samples (410, 626). SCGF level is significantly higher in vitreous fluids from patients with proliferative vitreoretinopathy or proliferative diabetic retinopathy with tractional RD than in rhegmatogenous RD or epiretinal membrane (639). Higher serum SCGF level is a risk factor for proliferative retinopathy in diabetic patients (685).
  Higher SCGF level in tear fluid from post-endothelial keratoplasty eyes of patients with bullous keratopathy or Fuchs’ endothelial dystrophy correlates with preexisting corneal haze and lower post-transplant visual acuity (612).
  Scgf gene expression is highly up-regulated in the lens epithelial cells from Dock5 mutant mice with rupture of lens cataract (572).
  SCGF protein is produced by trabecular meshwork of glaucoma patients (61). Scgf gene is up-regulated in the conjunctiva and Tenon capsule of a rat model of glaucoma 5-12 days after glaucoma filtering surgery to reduce intraocular pressure (59).
  Scgf gene expression is up-regulated in the orbital fat from patients with thyroid-associated orbitopathy (378).
  SCGF concentration presents no significant difference between extracts from ocular rosacea and normal skin tissues (386).

  Malignant melanoma (MM) cell lines, WM266-4 (160), UDCCS-1 and WDCCS-1 (161) produce SCGF, scgf+nestin+
mdr-1+ cells of which are estimated MM-initiating cells. Scgf gene expression is up-regulated in A375 MM cells 48 hours after in vitro treatment with 0.1 μM B-Raf kinase inhibitor Vemurafenib (499). When CD133 gene expression of human MM cells, FEMX-I is suppressed using CD133 nucleotide sequence 773-792-targeted shRNA, Wnt inhibitors and scgf genes are up-regulated as compared with untreated controls (162). CD133 is one of the markers of cancer stem cells. Down-regulation of CD133 reduces tumorigenic and metastatic ability of FEMX-I cells, consistent with up-regulation of Wnt inhibitors. Simultaneous scgf up-regulation implicates some compensatory mechanisms for proliferative activity of cancer stem cells. RNA-Seq analysis on MM cells showed that scgf gene expression in the MM cell lines (MeWo and 501Mel) and short-term cultured cells from 5 of 8 MM patients was similar to that in the control K562 cells (RPKM=2.23), but highly up-regulated in the cells from the rest 3 MM patients (RPKM=36.38, 21.48, 13.49) (238).
SNP ([c/t]rs13866) of scgf  gene is associated with susceptibility to vitiligo vulgaris (203). Vitiligo vulgaris is a depigmentary disease caused by extinction of melanocytes. Keratinocytes play a homeostatic role for epidermal-melanin unit by elaborating KL, bFGF, endothein-1, HGF and SCGF. Gene abnormality in the keratinocyte-derived growth factors has been one of the pathogenetic candidates of vitiligo vulgaris. The keratinocyte-derived growth factor genes from 51 cases of vitiligo vulgaris without autoimmune disease were compared with those from 118 normal controls. KL SNP (rs11104947: G/A) and scgf SNP ([c/t]rs13866) were associated with a 1.95- and a 2.14-fold higher susceptibility to vitiligo vulgaris, respectively, and the combined two gene SNPs further showed a 7.92-fold higher risk of developing the disease. Scgf independently or KL-dependently regulates a keratinocyte-melanocyte proliferative interaction, and scgf-dysregulation is associated with susceptibility to vitiligo vulgaris, for (1) scgf gene is expressed in neonatal or immature keratinocytes, (2) scgf SNP ([c/t]rs13866) is located at 3'UTR that is the target locus for hsa-miR-663, important for translation of scgf mRNA, and (3) scgf chromosomal locus 19q13.3 has been reportedly associated with vitiligo vulgaris. Association of vitiligo with scgf SNP [c/t]rs7246355 is in conflict; positive (203) and negative (303).
  When a healing process of dermal incision is disturbed by mechanical distraction, scgf gene expression is up-regulated in the skin wounds relative to the unloaded controls (351). SerumSCGF level is significantly higher in erysipelas patients at both acute and convalescent phases compared to healthy controls (568).
  Causal regulators active in the subcutaneous adipose tissue from obese individuals, TNFSF11 and CD34, up- and down-regulate scgf gene expression, respectively (383).
  SCGF is normally produced by fibroblasts from newborn patients with recessive dystrophic epidermolysis bullosa due to loss of collagen VII (421). However serum SCGF level is significantly up-regulated in patients with epidermolysis bullosa (677).