Our data showed that KLX was able to inhibit the upregulation of phosphorylated ERK1/2 expression significantly in mouse hearts after TAC operation, which indicated that TGF-β1/ERK1/2 noncanonical but not TGF-β1/Smads canonical pathway was involved in the antifibrosis effect of KLX on hearts of pressure overload mice (Figure 9). The gene discussed is MAPK3; the disease is persistent truncus arteriosus.