Based on these findings, Gal-1 and -8 may be considered therapeutic targets against viral infection and endothelial dysfunction in the lung microvasculature, against the severe immuno-thrombosis complication of the disease [77], or against trans-differentiation of lung fibroblasts into myofibroblasts, a crucial step in pulmonary fibrosis progression post-COVID-19 [68]. The gene discussed is LGALS1; the disease is COVID-19.