Ningetinib inhibited the phosphorylation of FLT3 and its downstream target proteins STAT5, AKT and ERK in a dose- and time-dependent manner, serving as the mechanism by which ningetinib has significant antileukemic effects on FLT-ITD-positive AML cells (Fig. 2A, B). The gene discussed is AKT1; the disease is acute myeloid leukemia.