We hypothesize that elevated pro-inflammatory cytokines might act in concert with those predisposing backgrounds, considering their increase in most MIS-C patients and possible sustenance by gene variants identified in the MIS-C patients and previously in autoinflammatory diseases associated with enhanced production of IFN-γ (32) [such as HLH or Blau syndrome (33)]. The gene discussed is IFNG; the disease is Blau syndrome.