Furthermore, acute MIS-C has recently been characterized by activated classical, alternative, and terminal complement pathways leading to elevation of C1s-C1-inhibitor complex and C4a and C4d levels, increased Bb and C3a concentrations, and elevation of sC5b-9, which were independent of anti-SARS-CoV-2 humoral immune response [18]. Here, C4A is linked to COVID-19–associated multisystem inflammatory syndrome in children.