This does indeed occur by various mechanisms in different cancers, including phosphorylation of AMPK‐α1 at Ser487 by Akt, which inhibits its subsequent phosphorylation at Thr172 and activation by LKB1 44, and degradation of AMPK‐α1 following polyubiquitylation by the E3 ligase TRIM28, which is targeted to AMPK by MAGE‐A3/‐A6; the latter were originally defined as tumour antigens normally only expressed in testis, but also aberrantly re‐expressed in many cancers 45. Here, PRKAA2 is linked to cancer.