These findings are consistent with previous observations indicating decreased mitochondrial respiration [9, 10], lower protein expression of key molecular markers of mitochondrial function and biogenesis, including citrate synthase and peroxisome proliferator‐activated receptor‐γ coactivator (PGC)1α [10] and higher glycolytic metabolites in skeletal muscle of PCC patients compared to controls [9]. This evidence concerns the gene PPARGC1A and adrenal gland pheochromocytoma.