Ang II infusion leads to activation of the renin angiotensin-aldosterone system and induces cardiac-remodeling characterized by cardiac fibrosis, hypertrophy, and dysfunction.30 Analysis of these end points after infusion with Ang II revealed greater cardiac remodeling in the mice that harbored HSPC with the Ppm1d mutation compared with the control nontargeted sgRNA group (Figure 2). This evidence concerns the gene PPM1D and fibrosis.