This early article refines the different mechanisms in which a galectin antagonist may treat SARS-CoV-2. Besides binding to the spike protein and preventing cellular entry, the article hypothesized a galectin inhibitor could modulate the host immune response, and reduce the incidence of pulmonary fibrosis. Gal-3 secreted by macrophages during injury promotes the upregulation of TGF-ß receptors, leading to fibroblast activation and collagen deposition (Delpino & Quarleri, 2020). Gal-3 inhibition has been shown to reduce adenovirus-induced lung fibrosis, and an inhibitor is currently in Phase IIb clinical trials for IPF treatment.