MIS-C transcriptional signature in blood also partially shares the transcriptional response to SARS-CoV-2 and the Kawasaki disease signature, with enrichment for exhausted CD8* T-cells and CD56dimCD57* natural killer cells, suggesting downregulation of natural killer cells and cytotoxic T cell exhaustion response to SARS-CoV-2 infection in MIS-C, with TBX21, TGFBR3, C1ORF21, S1PR5, PRF1, MYBL1, KLRD1, SH2D1B, and GZMA genes as the key drivers of MIS-C pathogenesis (Beckmann et al. 2021). This evidence concerns the gene PRF1 and COVID-19–associated multisystem inflammatory syndrome in children.