A direct role of Gal-3 in AF was demonstrated by its action in: (i) promoting the retention of cytokine receptors on the atrial myofibroblast membrane, through entrapment within Gal-3 lattice [70]; (ii) interaction of the extracellular pentameric Gal-3 with molecules, such as TGF-β, which could contribute to initiate fibrogenesis [79]; (iii) promoting nuclear translocation of transcription factors such as β-catenin. The gene discussed is LGALS3; the disease is atrial fibrillation.