Interestingly, the prolonged survival of virus-target cells did not increase viral replication but rather exacerbated inflammation as demonstrated by higher levels of key inflammatory mediators such as interleukin (IL)-6 (Groskreutz et al., 2007), i.e. key cytokine of the “cytokine storm” characterizing COVID-19 patients. This evidence concerns the gene IL6 and COVID-19.