Table 3 summarizes the available preclinical studies targeting TP53/p53 in AML in vitro and in vivo models. Finally, agents that can help overcome resistance to currently available therapies have also been investigated. Targeting mitochondrial metabolism with novel antimitochondrial agents, including electron transport chain complex inhibitors, pyruvate dehydrogenase inhibitors, and mitochondrial ClpP protease agonists has led to enhanced sensitivity of leukemic cells to combination treatment with VEN and AraC and substantially delayed relapse [118]. Here, TP53 is linked to acute myeloid leukemia.