Concurrently, the evidence of the association between galectin-3 and cardiac fibrosis in the heart failure is convincing, [37] but the association of AF and galectin-3 is unclear: according to some reports, galectin-3 is just a bystander in the fibrinogenesis of the heart, with overall co-morbidity, particularly obesity, as the real promoter of fibrosis, whereas some reports point out that even ‘lone AF’, i.e., AF without co-morbidities, increases galectin-3 values [40–43]. The gene discussed is LGALS3; the disease is Obesity.