In this study, using VEGFR‐3 knockdown (VEGFR‐3f/−) mice or wild‐type (WT) mice treated with a recombinant human VEGF‐C156S mutant, we examined the potential role of VEGF‐C‐VEGFR‐3 signaling in cardiac hypertrophy and dysfunction induced by transverse aortic constriction (TAC). Here, FLT4 is linked to persistent truncus arteriosus.