In conclusion, following an in vitro validation of our in silico predictions, the use of Gal-3 inhibitors could lead to a modulation of the host immune response and consequently the incidence of CSS, a reduction of the incidence of post-infection pulmonary fibrosis, and the prevention of viral entry, exploiting dual targets for both Gal-3 and spike protein. Here, LGALS3 is linked to pulmonary fibrosis.