The data showed that deletion of Hsp47 in cardiomyocytes or endothelial cells did not alter the otherwise robust development cardiac hypertrophy after pressure overload stimulation, yet Postn-MCM mediated deletion of Hsp47 from myofibroblasts resulted in a significant reduction in cardiac hypertrophy versus controls (Figure 5D). The gene discussed is SERPINH1; the disease is cardiac hypertrophy.