The miR-1-2 overexpression or Hand2 targeted knockout resulted in a similar embryonic lethality phenotype in mice, while miR-1-2 deletion led to a fourfold increase in Hand2 protein levels and homozygous lethality due to ventricular septal defects (VSD) [51, 52]. This evidence concerns the gene HAND2 and ventricular septal defect 1.