In this context, the t-tubule and Ca2+i transient abnormalities that we have observed as a result of reduced telethonin phosphorylation (through the partial replacement of endogenous bis-phosphorylated telethonin with a non-phosphorylatable variant) are similar to those that have been reported in multiple cardiac pathologies, including heart failure (27, 31), and, recently, in ventricular myocytes from telethonin knockout mice (29). This evidence concerns the gene TCAP and heart failure.