Studies have shown that HO-1 activation contributes to inhibiting the generation of proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 in pathophysiological conditions [62–65] and it has emerged as a key molecule for regulating inflammatory responses and oxidative stress in a variety of diseases, such as chronic fatigue syndrome, diabetes mellitus, hepatitis, and cancer [66]. The gene discussed is TNF; the disease is myalgic encephalomeyelitis/chronic fatigue syndrome.