On the one hand, treatment with low-dose (sublethal) chiglitazar inhibited the PI3K/Akt signaling pathway by activating PPARα, which co-operated with venetoclax to regulate the expression of BCL2 family proteins (including down-regulation of anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1, as well as up-regulation of pro-apoptotic Bim) in AML cells. The gene discussed is AKT1; the disease is acute myeloid leukemia.