Venetoclax is known to induce mitochondrial‐related apoptosis by blocking pro‐survival BCL2 proteins and inducing a caspase‐mediated proteolytic cascade.[22] Depletion of COX4I1 augmented the level of cleaved‐caspase 3 (c‐Cas 3; enzymatically active form) in venetoclax‐treated leukemia cells (Figure 6B). The gene discussed is BCL2; the disease is leukemia.