PRKAA2 and breast carcinoma: AMPKactivation ultimately results in downstream events that conserve cellular energy by inhibiting fattyacid synthesis while activating fatty acid oxidation as an alternative source of energy.Intriguingly, the ability of AMPK to coordinate the adaptive response of cellular bioenergetics toATP depletion may also be responsible, at least in part, for the reduced sensitivity ofHER2 gene-amplified breast cancer cells to HER-targeting drugs.