To test the hypothesis that eIF3a regulates AMPK activity, we took advantage of human non–small cell lung cancer (NSCLC) cell lines with (H1299, SW1573, and H226) or without (A549, H460, and H23) endogenous wildtype LKB1 and evaluated AMPK activation following eIF3a knockdown by assessing the phosphorylation of the AMPKα activation loop residue Thr172 and phosphorylation of its substrate acetyl-CoA carboxylase 1 (ACC1) at its Ser79. The gene discussed is PRKAA2; the disease is lung cancer.