A dysregulated immune response called a ‘cytokine storm’ (also known as ‘cytokine-release syndrome’) and characterized by an excessive increase in circulating levels of several pro-inflammatory cytokines (such as IL-1, IL-2, IL-6, IFN-γ and TNF) has been shown to play a central role in the pathophysiology of the most severe cases of COVID-19, leading to acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation, multiorgan failure and ultimately death [4,5]. This evidence concerns the gene IL2 and acute respiratory distress syndrome.