During the development of acute myocardial infarction, elevated Wnt2 promoted β-catenin/NF-κB signaling by binding to Fzd4 and LRP6, and elevated Wnt4 activated the same signaling by binding to Fzd2 and LRP6, resulting in a pro-fibrotic effect.149 Axis inhibition protein (Axin)/ adenomatosis polyposis coli protein (APC)/ glycogen synthase kinase 3 beta (GSK3β)/ casein kinase 1 alpha (CK1alpha) complex phosphorylates and inactivates β-catenin. This evidence concerns the gene NFKB1 and myocardial infarction.