Recently, an elaborate study comprehensively examined the expression of PDC component proteins and its regulatory proteins found the increased expression levels of E1α, diminished expression of PDK4, and indifferent levels of E1β, PDK1, and PDK2 in the myocardia of HF patients compared to the nonfailing heart, which support sustained adaptive capacity for PDC to facilitate glucose metabolism facing the energy deficiency condition in the failing heart (27). This evidence concerns the gene PDK2 and hydrops fetalis.