Previous studies have demonstrated that loss of LKB1 elevated glutamine uptake and flux in proliferative cells for biosynthesis and bioenergetic needs.25,63 Due to the potential preference of ESCC to glutamine metabolism and the dependency of cancer cells on glutamine supply,5,10 we speculated whether glutamine metabolism is involved in the tumor-promoting function of RBM4-LKB1 axis. Here, RBM4 is linked to esophageal squamous cell carcinoma.