The present study demonstrated that in the early stage of LVH without CKD, (i) not serum FGF23 but cardiac FGF23 levels significantly increased during LVH progression; (ii) cardiac FGF23 expression was lower in the heart than in the bone in the TAC group; (iii) serum aldosterone levels and cardiac ACE expression significantly increased and cardiac ACE2 expression significantly decreased in the TAC group; and (iv) ACEi could prevent LVH progression but FGF4Ri could not. The gene discussed is FGF23; the disease is persistent truncus arteriosus.