One possibility is that the constitutive absence of Gal-8 in Lgals8−/− mice triggers compensatory mechanisms that reduce damage, whereas the acute downregulation of endogenous Gal-8 in Lgals8+/+ mice, might result in the exacerbation of early AKI outcomes unless supplemented with exogenous Gal-8. Here, LGALS8 is linked to acute kidney injury.