We show that AML cells presenting a partial loss of DELE1 expression fail to activate the newly defined OMA1-DELE1-HRI pathway [10, 11] and downstream ATF4 signaling, resulting in a resistance to mitochondrial stress-induced apoptosis, and suggesting DELE1 as a new haploinsufficient driver gene that may contribute to −5/del(5q) AML phenotype. The gene discussed is OMA1; the disease is acute myeloid leukemia.