To examine the effect of AMPK activation on PCa, we made use of a conditional genetic gain-of-function AMPK mouse model harboring a mutation of aspartic acid residue 316 to alanine on the γ1 subunit.11,12 We crossed mice with prostate-specific deletion of Pten with mice expressing D316A γ1 specifically in prostate epithelial cells, using probasin-cre13 to generate Pten−/− and Pten−/−;AmpkACT. The gene discussed is PRKAB1; the disease is posterior cortical atrophy.