In a model of IgA nephropathy with renal fibrosis, Gal-3 deficiency led to reduced NLRP3 activation, lower IL-17 and IL-1β levels, and attenuation of fibrosis, whereas Gal-3 was found to promote T helper 17 (Th17) cell differentiation [12]. Here, LGALS3 is linked to IgA glomerulonephritis.