Although AP-1activation by AMPKα1 alone cannot affect cardiac function orhypertrophy, AP-1 may play a deleterious role in HF through multiple pathways.These findings suggest that AMPKα2 has a protective effect inboth normal and failing hearts, and the development of drugs that can alter orblock the reduced expression of AMPKα2 in the failing heartcould lead to a breakthrough in HF therapy. The gene discussed is PRKAA2; the disease is hydrops fetalis.