TNNI3K and cardiomyopathy: To identify downstream protein targets of Tnni3k phosphorylation and gain insights into the pathways regulated by the Tnni3k protein underlying the molecular mechanisms of aberrant tnni3k splicing-induced cardiomyopathy and CCD, we performed both quantitative proteomic and phosphoproteomic analysis using protein lysate isolated from the tnni3ke4/+ heterozygous mutant hearts, as the mimicking TNNI3K splice site variation identified from the human patient is a heterozygous mutation.