It has been shown that PGC-1α or PGC-1β null mice only exhibit mild phenotype, whereas mice bearing compound mutation of PGC-1α and PGC-1β die shortly after birth from heart failure, suggesting that both coregulators exert redundant functions, sharing roles that collectively are necessary for the postnatal metabolic and functional adaptation [32]. Here, PPARGC1B is linked to heart failure.