Ligand for the receptor-type protein-tyrosine kinase KIT. Plays an essential role in the regulation of cell survival and proliferation, hematopoiesis, stem cell maintenance, gametogenesis, mast cell development, migration and function, and in melanogenesis. KITLG/SCF binding can activate several signaling pathways. Promotes phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, and subsequent activation of the kinase AKT1. KITLG/SCF and KIT also transmit signals via GRB2 and activation of RAS, RAF1 and the MAP kinases MAPK1/ERK2 and/or MAPK3/ERK1. KITLG/SCF and KIT promote activation of STAT family members STAT1, STAT3 and STAT5. KITLG/SCF and KIT promote activation of PLCG1, leading to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. KITLG/SCF acts synergistically with other cytokines, probably interleukins.,Alternative sequence (3); Beta strand (5); Chain (2); Disulfide bond (2); Glycosylation (7); Helix (6); Natural variant (6); Sequence conflict (6); Signal peptide (1); Site (1); Topological domain (2); Transmembrane (1); Turn (2),Hyperpigmentation with or without hypopigmentation, familial progressive (FPHH) [MIM:145250]: A disorder characterized by hyperpigmented patches in the skin, present in early infancy and increasing in size and number with age. Hyperpigmentation has variable intensity, and sometimes is associated with cafe-au-lait macules and larger hypopigmented ash-leaf macules. {ECO:0000269|PubMed:19375057}. Note=The disease is caused by mutations affecting the gene represented in this entry.; Deafness, congenital, unilateral or asymmetric (DCUA) [MIM:616697]: An autosomal dominant form of non-syndromic, sensorineural deafness characterized by inability to hear affecting one ear. Some patients suffers from asymmetric, bilateral hearing loss. {ECO:0000269|PubMed:26522471}. Note=The disease is caused by mutations affecting the gene represented in this entry.