BCL2 and acute myeloid leukemia: Venetoclax can activate the endogenous mitochondrial apoptosis pathway, promote the release of inflammatory factors from immune cells, and cause tumor cell apoptosis.[29] Bcl-2 is highly expressed in AML progenitor cells, and Bcl-2 inhibitors may enhance the sensitivity of AML cells to demethylating drugs.[30] It has been confirmed in vitro that venetoclax and AZA have a synergistic antileukemia effect.[31] Mcl-1 is a protein from the Bcl-2 protein family and plays a key role in the survival of AML cells.