Although previous efforts mainly devoted to the studies of AMPK roles in LBK1 tumor suppressor functions, recently, depletion of AMPKα1 or AMPKα2 could not markedly impair LKB1 tumor suppressive roles in KRASG12D-driven NSCLC models,41 indicating that other substrates will play more important roles in mediating LBK1 tumor suppressor functions. The gene discussed is PRKAA2; the disease is neoplasm.