We would like to highlight three potential roles of gal3 in COVID-19 progression: (i) the macrophage-related hyperinflammation phase that drives the cytokine storm in most severe cases; (ii) the virus infection mechanism via the viral spike protein, given that its N-terminal domain has been suggested to evolve from a galectin origin (5); and (iii) the COVID-19-related lung fibrosis linked to the acute phase of diffuse alveolar damage, oedema, hypoxia, and inflammatory response. This evidence concerns the gene LGALS3 and pulmonary fibrosis.