The loosen cristae junction (i.e., widen cristae with reduced L‐OPA1 to S‐OPA1 ratio shown in Figure 3C,D) and the leakiness of mitochondria (increased cytochrome c release into cytosol observed in Figure 3E) induced by sgCOX4I1 preconditioned the AML cells as amendable to venetoclax (a BH3 mimetic) treatment, which primes cytochrome c release and the caspase‐mediated apoptosis through inhibiting the pro‐survival BCL2 proteins and activation of the pro‐apoptotic BAX/BAK proteins (Figure 6G).[2, 22]. The gene discussed is BCL2; the disease is acute myeloid leukemia.