Taking it a step further, consistent with the in vitro observations, the in vivo results also confirmed that the hypertrophic-related protein (ANP and BNP) and fibrotic-related protein (Collagen1, FN, MMP2/9 and α-SMA) expressions were increased in TAC-induced cardiac hypertrophy but reduced by PARP16 knockdown (Fig. 6a, b). The gene discussed is FN1; the disease is persistent truncus arteriosus.