While both LKB1 and CaMKK2 are known major upstream activators of AMPK (37, 59), we show here that LKB1 contributes to eIF3a regulation of AMPK in only LKB1-proficient NSCLC cells, whereas CaMKK2 does not in either LKB1-proficient or LKB1-deficient cells. Here, PRKAB1 is linked to non-small cell lung carcinoma.