Moreover, it has been found that CD84 is an essential survival factor for CLL, acting by activating a signaling cascade that involves CD84 tyrosine phosphorylation, EAT-2 recruitment, and increased AKT phosphorylation, resulting in BCL2 upregulation (21); importantly, this survival cascade also plays a pivotal role in AML pathophysiology (22). This evidence concerns the gene BCL2 and acute myeloid leukemia.