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 This evidence concerns the gene CCND1 and ventricular septal defect.