Our aims were to investigate its putative metabolic role by evaluating 1) PRL-mediated changes in CPT1 expression in breast cancer cells compared to normal breast epithelial cells at the mRNA and protein levels, 2) changes in CPT1 enzyme activity, and 3) activation of the AMPK pathway via phosphorylation of its α subunit at Thr172 and inactivation of ACC via phosphorylation at Ser79. This evidence concerns the gene PRKAA1 and breast carcinoma.