Finally, our results with G361 cells show that AMPK can still phosphorylate downstream targets such as ACC in response to energetic stress, even in LKB1 null tumor cells, although the effects may be smaller than those in LKB1-expressing cells in that they would rely entirely on allosteric activation, without any changes in Thr172 phosphorylation. This evidence concerns the gene PRKAA2 and neoplasm.