Importantly, rWNT5A protein treatment could reverse Cthrc1 deficiency-induced post-MI cardiac rupture, which further supports that CTHRC1 promoted post-infarction cardiac repair via selectively activating non-canonical WNT5A-PCP signaling pathway other than canonical WNT3A-β-catenin signaling axis. The gene discussed is WNT3A; the disease is myocardial infarction.