CCND1 and ventricular septal defect 1: It has been reported that miR‐133a‐deficient hearts show increased and aberrant cardiomyocyte proliferation throughout the atria and ventricles; this latter result potentially explains the development of a lethal ventricular septal defect in miR‐133 knockout mice, where miR‐133a regulates several transcription factors involved in cell cycle control such as cyclin D1, which we found overexpressed in progenitor cells.28