Knock-down of B4GALT5 decreases the conversion of cardiac fibroblast into myofibroblasts with contractile properties and reduces collagen deposition, whereas overexpression of B4GALT5 elevates cardiac fibroblast activation and regulates the Akt/GSK-3β/β-catenin pathway to promote elevated fibrosis during heart failure [42]. This evidence concerns the gene B4GALT5 and heart failure.