The study has show that myocardial calcitonin levels aresix times higher in AF patients than in normal subjects and are involved inpathways related to fibrogenesis, infection and immune response, andtranscriptional regulation, and that atrial cardiomyocytes are also an activesource of calcitonin; restoration of impaired myocardial calcitonin-calcitoninreceptor signaling may offer a new strategy to inhibit atrial remodeling [46].Different neurohormonal-immune interactions can show favorable or maladaptiveresponses in cardiac remodeling. Here, CALCA is linked to atrial fibrillation.