In the present study, we utilized a canine model of nonischemic HF to test the hypothesis that the HF-related changes in RyR2 phosphorylation levels were mediated by the disruption of phosphatase activity localized to RyR2s due to enhanced expression of the two most abundant muscle-specific miRNAs, miR-1 and miR-133 [28]. This evidence concerns the gene RYR2 and hydrops fetalis.