A large body of literature supports that prolactin (PRL) released from the anterior pituitary gland promotes cell proliferation, survival, migration/invasion and angiogenesis.82 In MCF-7 and MDA-MB-231 breast cancer cells, recent study showed that PRL stimulation increased the expression of CPTIA (liver isoform) at both mRNA and protein level, and PRL-mediated effects are partially dependent on the LKB1-AMPK pathway.53 This result suggests that PRL may enhance fatty acid β-oxidation by stimulating CPTI expression and/or activity in breast cancer cells (Figure 3). This evidence concerns the gene STK11 and breast carcinoma.