An increasing interest in targeting mitochondrial function was proposed in AML therapy.[28] For example, it has been reported that disruption of mitochondrial ultrastructure could sensitize AML to venetoclax, a standard‐of‐care medication assigned for chronic lymphocytic leukemia (CLL) and AML patients.[15, 22] Our study revealed that genetic targeting COX4I1 facilitates the cellular apoptosis induced by venetoclax (Figure 6A–F), which could be attributed to the distorted mitochondrial architecture in the COX4I1 deficient AML cells (Figure 3B). The gene discussed is COX4I1; the disease is acute myeloid leukemia.