Further study of the genes we have identified in these screens will provide additional insight as to how PAR-4/LKB1 signalling blocks tumour growth by regulating cell cycle arrest under energetic stress, while providing additional LKB1 or AMPK downstream kinase substrates that could be useful for the development of new therapies to benefit PJS patients or other cancers that arise due to the loss of LKB1 function. This evidence concerns the gene STK11 and cancer.