KIT is a receptor tyrosine kinase that responds to stem cell factor (SCF/KITLG) binding and regulates cell survival, proliferation, and migration across multiple physiological systems 1. Upon SCF binding, KIT autophosphorylates and activates intracellular signaling cascades including PI3K/AKT, MAPK/ERK, and JAK/STAT pathways 1. KIT is essential for hematopoiesis, gametogenesis, mast cell development, and melanogenesis 2, with CREB transcription factor maintaining KIT expression in skin mast cells through a positive feedback loop 3. The SCF/KIT axis regulates oocyte and spermatogonial development, with hormonal dysregulation contributing to infertility 4. Gain-of-function KIT mutations drive multiple malignancies. In gastrointestinal stromal tumors (GISTs), mutations between the transmembrane and kinase domains cause constitutive KIT activation without SCF stimulation, driving transformation 5. Dysregulated KIT—from overexpression or mutation—promotes tumor progression, cancer stemness, epithelial-mesenchymal transition, and metastatic disease 1. KIT-positive cancer stem cells exhibit enhanced self-renewal, proliferation, migration, and chemotherapy resistance 6. Tyrosine kinase inhibitors targeting KIT show efficacy in c-KIT-positive malignancies, though drug resistance emerges 1. KIT mutational status predicts therapeutic response and clinical outcomes 7, making KIT a critical biomarker and therapeutic target in oncology.