Mechanistically, this may be due to redundancy across the GAB family member genes (Gab1, Gab2, Gab3, and Gab4), with previous studies suggesting that Gab1 (the most ubiquitously expressed family member) may be redundant with Gab2 in cardiac muscle, while Gab3 appears to have redundant function with Gab2 in immune cells (59, 70–72); regardless, only GAB2 inactivation shows a deleterious effect in AML cell lines. The gene discussed is GAB4; the disease is acute myeloid leukemia.