PRKAA1 and posterior cortical atrophy: In previous studies using this model, we did not observe any overt phenotype in control mice with global or tissue-specific expression of WT γ1 because these mice showed no change in AMPK expression or activity relative to non-transgenic mice.11,12,14 Consistent with our previous studies, we found no differences in PCa disease progression between Pten−/− and Pten−/−;AmpkWT mice (Figure S1A), and we therefore combined Pten−/− and Pten−/−;AmpkWT mice to generate a single control group, referred to as Pten−/− mice.