Overexpression of NAP1L2 significantly inhibited the global H3K27ac and NAP1L2 actually recruited SIRT3 which reduced the level of H3K27ac around the promoters of BCAT2 and PP2Cm, thereby leading to catabolic defect of BCAAs during the pathogenesis of DCM. This evidence concerns the gene NAP1L2 and familial dilated cardiomyopathy.