During AML progression, mutations in epigenetics regulators (e.g., DNA methylation-related genes DNMT3A, TET2, and IDH1/2), RNA splicing factors (e.g., SRSF2, U2AF1, and SF3B1), and chromatin modifiers (e.g., ASXL1, EZH2, and BCOR) often occur early [18], affecting self-renewal and differentiation, whereas mutations in signaling pathway genes (e.g., NRAS, KRAS, KIT, PTPN11, and FLT3) arise later [18]. The gene discussed is KIT; the disease is acute myeloid leukemia.