At the molecular level, HF evolution is characterized by a maladaptive down-regulation of the adult cardiac muscle proteins isoforms such as alpha myosin heavy chain (αMHC) and sarcoplasmic reticulum Ca2+-ATPase 2a (Serca2a) and a concomitant up-regulation of the fetal genes such as beta myosin heavy chain (βMHC) and phospholamban (Pln) (2). The gene discussed is PLN; the disease is hydrops fetalis.