RBM4 and esophageal squamous cell carcinoma: AMPK, the canonical substrate of LKB1, is a well-known metabolic hub that was previous reported to negatively affect glutaminolysis via its kinase activity.23,66 To assess whether AMPK is involved in the RBM4-regulated glutamine metabolism, we measured the glutamine flux by the addition of Compound C, an ATP-competitive AMPK inhibitor, in RBM4-knocked down ESCC cells.