In the present work 1) we described the association of individual TNNT2 mutations with AF by revising the clinical atrial data from 45 TNNT2-HCM index patients 2) to clarify the cellular basis of atrial pro-arrhythmogenic substrate we studied the energetics, mechanics and contractility of atrial myocardium from two well known HCM mouse models expressing TNNT2 mutations (R92Q and E163R) selected because of their likely different association to AF. The gene discussed is TNNT2; the disease is atrial fibrillation.