Myo-Inositol (myo-Ins), key molecule participating in several intracellular signaling pathways and physiological processes, has been proven to modulate interleukin-6 (IL-6) levels in chronic inflammatory diseases and to possess endothelial protective properties. Moreover, myo-Ins promotes the maturation of pulmonary surfactant phospholipids, with beneficial effects in the treatment of premature infants with respiratory distress syndrome (RDS). On these premises, myo-Ins has a potential application in the treatment of pulmonary diseases, and it could be successfully used to reduce the complications related to the SARS-CoV-2 pandemic event. Though information about the virus is still scarce, it is becoming evident that the Coronavirus infection triggers an interstitial pneumonia that quickly evolves into a severe RDS, associated with a thrombotic and vascular disease targeting endothelial cells throughout the body. These effects are most probably driven by a disastrous overreaction of the immune system, known as “cytokine storm”, which interests not only lungs but also gut, kidneys, heart, and brain, with platelet-endothelial dysfunction and abnormally rapid life-threatening blood clotting. Given the pathophysiology of the SARS-CoV-2 disease (COVID-19), it could be worth investigating whether myo-Ins properties can mitigate the disease-related complications in terms of surfactant production, modulation of inflammatory cytokines and endothelial protection.