Annexin A6 for example is the most abundant annexin expressed in the heart and its overexpression in mice has been shown to cause physiological alterations in contractility leading to dilated cardiomyopathy, while Annexin A6 knockout has been found to induce faster changes in Ca2 + transience and increased contractility71,72. This evidence concerns the gene ANXA6 and dilated cardiomyopathy.