Moreover, in these settings, in addition to the bone alterations already mentioned, the mice had progressive and hypertension-independent cardiac hypertrophy with an increased heart rate; these elements allowed the scientists to conclude that, among the NPs, CNP has a starring role at the cardiac level, and that NPR-B (unlike NPR-A) is the receptor most implicated in the failed heart [97]. The gene discussed is NPR2; the disease is cardiac hypertrophy.