Coronaviruses are the largest viruses with a positive-sense single-stranded-RNA genome. The host immune response is by one side essential for the resolution of COVID-19 infection, but it can also be crucial for the pathogenesis of major clinical manifestations of the disease. The angiotensin-converting enzyme 2 (ACE2) has been identified as the host cell-surface receptor for SARS-CoV2 envelope spike glycoprotein [12]. ACE2 is a type I membrane protein expressed on cells in the kidney, heart, gastrointestinal tract, blood vessels, and, importantly, lung AT2 alveolar epithelial cells, which are particularly prone to viral infection [13]. SARS-CoV-2 infection leads to the downregulation of ACE2 expression, thus resulting in excessive production of angiotensin II by the related enzyme ACE. It has been suggested that the stimulation of type 1a angiotensin II receptor (AGTR1A) increases pulmonary vascular permeability, thus potentially explaining the increased lung damage when the expression of ACE2 is decreased [14]. Due to this mechanism of action, it has been postulated that subjects with diabetes mellitus or hypertension using ACE-inhibitors or angiotensin receptor blockers may have an increase of both the risk of infection and the severity of COVID-19 [15]. As only scarce evidence supports this hypothesis, the European Society of Cardiology recently published a position statement that strongly recommends continuing these treatments despite the current epidemic [16]. An additional point to be clarified is also the role of the genetic predisposition for an increased risk of SARS-CoV-2 infection due to ACE2 polymorphisms that have been linked to hypertension, diabetes mellitus, and cerebral stroke, especially in Asian populations [15].