As venetoclax decreases OXPHOS [25,29], inhibition of energy metabolism by both the RUNX1 mutation and treatment with venetoclax may result in enhanced apoptosis, and this might explain the fact that RUNX1-mutated AML patients with an adverse risk and poor response to standard treatment have increased response rates to venetoclax-based therapy [4]. Here, RUNX1 is linked to acute myeloid leukemia.