However, when hemodynamic stress is a consequence of pathologies such as diabetes mellitus type 2, cardiac ischemia, obesity, or hypertension, cardiac cells undergo genetic and epigenetic changes that stimulate a pathology-induced stress program that includes increased expression of brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and β-myosin heavy chain (β-MHC), which accomplish pathological and adaptive roles [1–3]. The gene discussed is NPPA; the disease is obesity due to melanocortin 4 receptor deficiency.