From a physiological perspective, molecular mechanisms of mitochondrial energy deficits, inflammation with elevated IL6 and TNF, oxidative stress, hypothalamic-pituitary adrenal axis dysfunction, autonomic dysfunction, obesity and adipokine inflammation, and other processes may contribute to fatigue in a wide variety of chronic autoimmune, neoplastic, infectious, cardiac, pulmonary, joint, brain, kidney, and other disease settings (Matura et al., 2018). This evidence concerns the gene IL6 and obesity due to melanocortin 4 receptor deficiency.