From a molecular point of view, the zebrafish model of COVID-19 allowed to demonstrate that the hyperinflammation triggered by the S protein requires activation of both the Tlr2/Myd88 (Toll-like receptor 2/Myeloid differentiation primary response 88) and inflammasome signaling pathways, independent of IL1β production [202]. The gene discussed is TLR2; the disease is COVID-19.