In animal models of PO-induced hypertrophy and systolic dysfunction; the ratio of BAX to BCL-2 is increased as early as one week after PO and remains about the same thereafter until the development of HF; whilst, BNIP3 expression increases at 2–3 weeks after PO and peaks at HF development [14], therefore amplifying and potentiating mitochondrial dysfunction and the apoptotic process [13]. The gene discussed is BAX; the disease is hydrops fetalis.