While cardiac tissues co-express PRKD1, PRKD2, and PRKD3, and previous studies show that PRKD isoforms can be activated in a stimulus-specific manner in cardiomyocytes (Guo et al., 2011), most studies have focused on the cardiac actions of PRKD1, which is downregulated during normal postnatal development, upregulated in various cardiac hypertrophy/failure models, and contributes to adverse cardiac remodeling and has been implicated in syndromic congenital heart defects (Speliotes et al., 2010; Johnson et al., 2015). This evidence concerns the gene PRKD1 and congenital heart disease.