A recent in vitro study has shown that the p65 subunit of NF-κB directly represses PGC-1α activity in cultured cardiac cells, thereby leading to a reduction in PDK4 expression and the subsequent increase in glucose oxidation observed during the proinflammatory states such as chronic ischaemia, cardiac hypertrophy, and HF [115]. The gene discussed is PPARGC1A; the disease is hydrops fetalis.