Such critical courses of SARS-CoV-2 infection are thought to be driven by the so-called “cytokine storm” [3], an exaggerated response of the host immune system that induces the release of proinflammatory cytokines and chemokines, namely interleukin (IL)-1, IL-6 and tumor necrosis factor-a (TNF-a), as observed in macrophage activation syndrome (MAS) or secondary hemophagocytic lymphohistiocytosis (sHLH) [4,5]. This evidence concerns the gene TNF and secondary hemophagocytic lymphohistiocytosis.