However, in the case of moderate or severe COVID-19, high viral load and/or individual immunogenetic factors alter the immune landscape; low levels of antiviral interferons and several cytokines (IL-1β, IL-2R, IL-6, IL-7, IL-8, IL-17, and TNF-α) and chemokines (CCL-2, CCL-3, CCL-5, CCL-7, CXCL-10) are produced, and a systemic or/and diffuse pulmonary hyper-inflammatory state develops as a sequela [39,40]. The gene discussed is IL6; the disease is COVID-19.