Previous work in the MRC Unit has suggested that activating the AMPK pathway using clinically approved anti-diabetes drugs such as metformin could be employed to suppress tumour formation. This would inhibit cell growth by tricking a cancer cell into believing that it did not have enough energy to grow. Xu tested this idea by administration of tumour prone PTEN+/- mice with metformin as well as 2 other drugs that activate AMPK (phenformin or A-769662). He found that these drugs markedly activated AMPK in mice tissues and lead to significant delays in the onset of tumour formation in these mice. Xu also showed that inhibiting the AMPK pathway by reducing the expression of LKB1 markedly accelerated the rate at which tumours arose in PTEN+/- mice. The paper describing these findings has just been published in the Biochemical Journal. These findings highlight in an animal model relevant to understanding human cancer, the vital role that activation of the LKB1-AMPK pathway plays in suppressing tumourigenesis resulting from loss of PTEN tumour suppressor. Xu's study demonstrates that the clinically approved diabetes drug metformin as well as its more potent derivative phenformin have great potential in suppressing cancer. They suggest that metformin or phenformin could be used to prevent onset of tumours and suggest that further work into whether these drugs would have benefit for the treatment of cancer would be worthwhile.