Consistent with this, we verified that LKB1-depletion was capable of rescuing the RBM4 depletion-induced inhibition of the glutamine consumption, and glutamate production (Fig. 6h), whereas in RBM4 stably overexpressing ESCC cells, re-expression of LKB1 overturned the upregulated consumption of glutamine and the high rate of glutamate production (Supplementary Fig. 5a). The gene discussed is RBM4; the disease is esophageal squamous cell carcinoma.