One possible scenario is that mitochondrial deficits shared by both twins may underlie the pathogenic mechanisms leading to the neurological symptoms present in both children (depression, mood instability, ADHD), whereas others (e.g., a more severe OXPHOS deficit, higher mitochondrial ROS production, repression of PGC-1α/β) may associate with the bipolar disorder, maniac behavior, and chronic fatigue diagnosed solely in twin 2. This evidence concerns the gene PPARGC1A and depressive disorder.