Mechanisms involved in this negative progression are mainly: (a) higher expression of ACE2 in the lung, increasing the likelihood of spreading of the virus [119]; (b) unbalanced ACE2/ACE ratios with consequent increased inflammatory and oxidative stress responses [120]; (c) high glucose concentrations in the fluid lining the lungs favouring viral replication [121]; (d) endothelial dysfunction with higher pro-thrombotic risk [122]; (e) higher predisposition of developing respiratory infections [123]. The gene discussed is ACE2; the disease is endothelial dysfunction.