For example, in the presence of CCAAT/enhancer-binding protein alpha (CEBPA) mutations, the ASXL1-G643W variant accelerates AML progression and chemotherapy resistance by downregulating key leukemia-related pathways, including ribosome biosynthesis, regulation of DNA damage response via p53 mediators, and immune activation [42]. The gene discussed is CEBPA; the disease is acute myeloid leukemia.