The accelerated progression of DCM observed in Lrrc10−∕− mice after pressure overload indicates that deletion of LRRC10 renders the heart sensitive to disease pathogenesis during hypertensive remodeling, suggesting that human patients with mutations in the LRRC10 gene may be prone to more fulminant disease and DCM under conditions of pressure overload, such as aortic stenosis or elevated blood pressure. This evidence concerns the gene LRRC10 and aortic stenosis.