It can be argued that in all of the mouse studies where a tumour suppressor role was supported (e.g. in the Eμ-Myc model of B-cell lymphoma [163], the p53-null [166] and PTEN-null [167] models of T-cell lymphoma and the PTEN-null model of prostate cancer [170]), AMPK function had been knocked out prior to tumorigenesis. Here, PRKAA2 is linked to prostate carcinoma.