Nonetheless, as advocated by recent studies on DELE1 characterization [10, 11, 29], the influence of its pathways on chemotherapeutic treatments of other tumor types [33], and given the advantage of cells able to cope with mitochondrial perturbation through modification of OMA1-DELE1-HRI signaling, a modulation of this pathway could represent an attractive therapeutic avenue worthing further investigations, especially in the −5/del(5q) AML context which represents a major challenge in terms of clinical management. The gene discussed is DELE1; the disease is acute myeloid leukemia.