Though a decline in PGC1 isoforms (PGC1α and PGC1β) is noted in other metabolic diseases, such as obesity and diabetes [28–31]; it is generally accepted that deacetylation, and not the changes in the expression level, of PGC1α is required for maintaining the mitochondrial biogenesis. The gene discussed is PPARGC1A; the disease is obesity due to melanocortin 4 receptor deficiency.