It also induced apoptosis in the human acute myeloid leukemia cell line HL-60 through comcomitant enhancement of caspase-3 activity and DNA fragmentation, significantly decreasing the nuclear entry of NF-κB p65, suppressing NF-κB activation, and inhibiting the expression of Bcl-xL and X-linked inhibitor of apoptosis protein (XIAP) [56]. Here, BCL2L1 is linked to acute myeloid leukemia.