However, hAG+/+ females lacking ATII receptor type 1a (mAT1a) mated with hRN+/+ male mice (pregnant hAG+/+/mAT1a−/−) have a normotensive phenotype, and the placental abnormalities, maternal cardiac hypertrophy, and IUGR are ameliorated [85]. Here, MAT1A is linked to fetal growth restriction.