investigated the molecular mechanism of glabridin’s anti-cancer effects in human promyelocytic leukemia and found (89) that glabridin upregulates the phosphorylation of P38 MAPK and JNK1/2 in a time- and dose-dependent manner, promoting the activation of caspase-3, caspase-8, and caspase-9, thereby inhibiting the proliferation of acute myeloid leukemia (AML) cell lines (HL-60, MV4-11, U937, and THP-1). This evidence concerns the gene CASP9 and acute myeloid leukemia.