Previous work has suggested that FAO could be involved in BCL2 regulation and BAX- and BAK-dependent mitochondrial permeability transition pore formation through interactions between CPT1 and the pro-apoptotic BH3-only protein Bid [130] or BCL2 [131], highlighting a dual interest in FAO inhibition and synergy with BH3 mimetics in AML. The gene discussed is CPT1A; the disease is acute myeloid leukemia.