In Tgαq*44 mice, initially developed by Mende et al. [40], cardiomyocyte-specific overexpression of the constitutively active Gαq protein imitates excessive neurohormonal drive in the heart and results in slowly progressing cardiac pathology that mimics HF in humans on molecular, morphological, phenotypic and functional levels [40, 42, 53, 63–67]. This evidence concerns the gene GNAQ and hydrops fetalis.