Our findings are in line with clinical evidences showing that an increase in gene dosage at the IFNR cluster locus in patients with Down syndrome is associated with a decreased lifelong risk of developing solid tumors at the expenses of a pro-senescent cellular phenotype and a proinflammatory milieu, resulting in a higher risk of incidence of systemic inflammatory and autoimmune diseases33–36. The gene discussed is IFNAR2; the disease is Down syndrome.