Constitutive activation of IFN signaling could conceivably explain a large number of comorbidities associated with DS, such as the increased risk of transient myeloproliferative disorder, diverse leukemias, several autoimmune disorders (Richardson et al., 2011), and perhaps even the lower rate of solid tumors (Zitvogel et al., 2015; Hasle et al., 2016). The gene discussed is IFNA1; the disease is leukemia.