Given that RPTOR could rescue the phosphorylation level of ULK1 and reduce autophagy in METTL1 knockdown ESCC cells, we next knocked down ULK1 in METTL1 depleted ESCC cells to determine whether METTL1 and RPTOR promote ESCC progression via regulation of ULK1-mediated autophagy (Fig. 4i and Supplementary Fig. 8h). This evidence concerns the gene ULK1 and esophageal squamous cell carcinoma.