Ectopic overexpression of constitutively active PKD1 in mouse heart leads to cardiac hypertrophy [14], [15], [16], while cardiac-specific deletion of PKD1 in mice suppressed pathological cardiac remodeling in response to various stress stimuli and significantly improved cardiac function [13], indicating a critical role of PKD in this pathological process. Here, PRKD1 is linked to cardiac hypertrophy.