In COVID-19 pneumonia there is an accumulation of monocytes/macrophages and T-cells in the lungs with local overproduction of pro-inflammatory cytokines causing lung damages and possibly multi-organ failure related to the cytokine storm [2, 7], although the peak of serum cytokines (i.e. IL-6, IFNγ) in severe/critical COVID-19 patients was significantly lower than in other clinical conditions (i.e. sepsis, cytokine release syndrome (CRS) in the setting of chimeric antigen receptor (CAR) T-cell therapy, hyperinflammatory Acute Respiratory Distress Syndrome) [8]. This evidence concerns the gene IL6 and COVID-19.