The important findings suggest that SIRT1 and/or elements downstream in the OXPHOS pathway may be potential therapeutic targets, for instance, inhibiting PPARγ coactivator-1α (PGC-1α) by SR-18292 in combination with TKIs could avoid CML relapse by the increase in on PGC-1 acetylation levels affected of SIRT1 [106]. Here, PPARGC1A is linked to chronic myelogenous leukemia, BCR-ABL1 positive.