In myosin peptide-induced experimental autoimmune myocarditis (EAM) on C57Bl/6 mice, Galectin-3 KO mice developed more severe myocardial inflammation and more conspicuous hypertrophy, due to the accumulation of T helper type 2 (Th2) cells and expansion of type 2 inflammation in the hearts of otherwise predominantly Th1 C57Bl/6 mice. The gene discussed is LGALS3; the disease is autoimmune myocarditis.