The partial recovery of CPT1 enzyme activity in response to PRL in breast cancer cells suggests that AMPK activation may directly affect the expression of genes involved in modulating lipid catabolism, thereby contributing to changes observed at the level of CPT1 in a manner independent of ACC inactivation and a lift in the allosteric inhibition due to changing malonyl CoA levels. This evidence concerns the gene PRKAA1 and breast carcinoma.