Similar to GDM, MO human placentas present mitochondrial dysfunction, i.e., disrupted biogenesis (evidenced by decreased PGC-1α protein expression levels and decreased citrate synthase activity) [50] and bioenergetics (decreased complex-I activity and decreased ATP levels) [50,51], excessive ROS formation and oxidative damage (MDA and protein carbonylation increased levels, increased DCF fluorescence) [50,51,52], and lower antioxidant defenses (decreased SOD activity, decreased GPx-4 expression levels) [50,53], either in human whole placental tissue or in cytotrophoblasts (Figure 1). The gene discussed is PPARGC1A; the disease is gestational diabetes.