The addition of the BCL-XL inhibitor A133825, the MCL1 inhibitor S63845 or the PI3K inhibitor bimiralisib to venetoclax induced substantial reductions of cell viability in 50–70% of the tested AML samples, while the addition of the MEK inhibitor trametinib, the BMI-1 inhibitor PTC596 or the STAT3 inhibitor C-188-9 to venetoclax was less effective, with substantial reductions of cell viability in 20–40% of tested AML samples. This evidence concerns the gene BCL2L1 and acute myeloid leukemia.