Moreover, both association and dissociation of Ang II and the NP system with markers of oxidative stress, blood pressure, maladaptive immune and inflammatory response, cardiac hypertrophy and fibrosis have all been reported in the context of preclinical DD and HF resulting from mechanical overload, genetic models of leptin resistance, and inappropriate activation of the RAAS [22, 24, 48–50]. The gene discussed is LEP; the disease is cardiac hypertrophy.