NFKB1 and myalgic encephalomeyelitis/chronic fatigue syndrome: Morris et al. [59] suggested that increased Nuclear Factor kappa B (NF-kB), causing the release of pro-inflammatory cytokines, and decreased tumor suppressor protein p53, causing aerobic mitochondrial dysfunction, are the key mechanisms in ME/CFS associated with the increased production of reactive oxygen species (ROS), mitochondrial exhaustion, and the additional need for ATP production.