These results may explain (at least partially) that macrophage accumulation early after TAC is not due to the secondary effects induced by cardiac injury, but that the increase in MCP-1 immediately after TAC as a result of afadin-modulated regulation of TGFβ signaling in cardiomyocytes is involved in the promotion of macrophage infiltration in the heart. Here, TGFB1 is linked to persistent truncus arteriosus.