AML cases involve complex gene mutations and heterogeneous combinations of chromosomal alterations 3, such as mutations or abnormal expressions of N‐RAS, FLT3, CEBPA, PLSCR1 and so on 3, 4, 5, 6, 7, highlighting the difficulty in illuminating the pathogenesis of AML and developing specific therapy targets and drugs. The gene discussed is PLSCR1; the disease is acute myeloid leukemia.