{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nStem cell factor (SCF), also known as KIT ligand (KITLG), is a pleiotropic cytokine that regulates tissue regeneration, neovascularization, and hematopoietic reconstitution. In the injured brain and in malignant gliomas, KITLG is up‐regulated and directly activates endothelial cells to promote angiogenesis, while in the bone marrow niche, both adipocytes and stem/stromal cells produce KITLG to support hematopoietic regeneration and expand multilineage progenitors. Moreover, KITLG enhances differentiation of human embryonic stem cells toward the hematopoietic lineage and, when provided in transgenic models, improves myeloid development, endothelial progenitor cell recruitment, and even dental pulp tissue remodeling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n \nIn the realm of pigmentation and melanocyte biology, KITLG exerts a central role by controlling the survival, proliferation, and migration of melanocytes. Regulatory alleles in KITLG have been linked to pigmentation changes across vertebrates—ranging from reduced expression that produces lighter skin or blond hair in human populations and fish to misexpression observed in hyperpigmented skin lesions. Such alterations in KITLG regulatory regions, whether inherited or acquired, underlie classic pigmentation phenotypes and familial pigmentary disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "13"}]}, {"type": "t", "text": "\n \nKITLG also plays multifaceted roles in tumorigenesis and developmental disorders. Genetic variants and polymorphisms within regulatory elements of KITLG are associated with increased risks for testicular germ cell tumors, uveal melanomas, gastrointestinal stromal tumors, pancreatic cancers, and even chemoresistance in mesothelioma and lung cancer stem cells. In addition, aberrant KITLG signaling—whether through p53‐responsive enhancer mutations, POU3F2‐mediated up‐regulation in melanoma, or HIF‐1–dependent induction in hypoxic tumor microenvironments—has been implicated in promoting proliferation, invasion, and the survival of malignant cells. These oncogenic and developmental effects extend to conditions such as testicular dysgenesis and congenital hearing loss as observed in certain syndromic presentations."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "28"}]}, {"type": "t", "text": "\n \nBeyond its roles in tissue regeneration, pigmentation, and cancer, KITLG influences immune cell function and cellular survival via complex signal transduction cascades. Reviews of c-Kit signaling emphasize that KITLG is crucial for mast cell development and activation, operating in synergy with antigen‐mediated signals to enhance degranulation and cytokine production. Additionally, KITLG provides protection against apoptosis in progenitor cells—thereby safeguarding erythroid precursors during cytotoxic stress—and contributes to neuroprotection in cortical neurons. In the developing ovary, activin modulates KITLG expression to indirectly influence germ cell survival and primordial follicle formation, while heightened KITLG-related cytokine networks are implicated in disorders such as Langerhans cell histiocytosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lixin Sun, Ai-Min Hui, Qin Su, et al. 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