The pathogenesis of MIS-C is still insufficiently tested, but there are some hypothesis about this viral-associated autoimmune response: (1) molecular mimicry; (2) viral inducted epitope spreading; (3) liberation of self-antigens; (4) lower neutralization capacity (elevated antispike IgG and low antispike IgM levels); and (5) superantigens [1]. The gene discussed is CD40LG; the disease is COVID-19–associated multisystem inflammatory syndrome in children.