This theory was primarily based on the finding that in several cases of MEPPC and DCM due to gain-of-function SCN5A-R222Q variant, therapy with hydroquinidine, flecainide, or amiodarone (in addition to standard treatment of heart failure) rapidly and effectively reduced the number of multifocal premature ventricular contractions and reversed the LV remodeling [10,16,38]. The gene discussed is SCN5A; the disease is heart failure.