“…The pathogenesis of KD remains unclear, but the postinfectious nature of MIS-C, and possibly also of KD, is consistent with an autoinflammatory and/or autoimmune hyperinflammatory process initially triggered by viral infection ( Rowley et al, 1997 ; Rowley et al, 2020 ). The immune response in patients with KD is typically characterized by pro-inflammatory signatures, including increases in IL-1, IL-8, IL-6, and IL-17A levels ( Bajolle et al, 2014 ; Nelson et al, 2020 ; Oates-Whitehead et al, 2003 ), marked leukocytosis, eosinophilia, and high levels of monocytes ( Kanegaye et al, 2009 ; Radia et al, 2020 ), accompanied by high CRP, erythrocyte sedimentation rate, procalcitonin, alanine aminotransferase, and Îł-glutamyl transferase levels ( Henderson et al, 2020 ; Radia et al, 2020 ). Many of these features are common to MIS-C (including high levels of cytokines, such as IL-1, IL-8, IL-6, etc.…”