As a specific Bcl-2 inhibitor, venetoclax effectively induces apoptosis in vitro in cancer cells that overexpress Bcl-2.[85] In a time- and concentration-dependent way, Yuan et al found that venetoclax and HHT worked in concert to suppress AML growth, lower mitochondrial membrane potential, and accelerate AML cell death. Here, ACVRL1 is linked to acute myeloid leukemia.