SIRT5 inhibition resulted in increased POLRMT succinylation, which in turn led to a reduction in mtDNA binding and the expression of mtDNA-encoded genes, suggesting that SIRT5 inhibitors can be used for targeting mitochondria biogenesis in the course of the treatment of FLT3-mutant AML. The gene discussed is SIRT5; the disease is acute myeloid leukemia.