Previous researches proved that G6PD can be methylated and promoted translation by m6A ‘readers’ at 3’-UTR to promotes lung cancer cell growth [29], therefore we detected m6A level in G6PD (Fig. S1B) and found that it significantly up-regulated after METTL14 overexpression (Fig. 6D), whereas knockdown METTL14 reversed this phenotype (Fig. 6E) in consistent with lower binding at 3’-UTR of G6PD (Fig. 6F). Here, METTL14 is linked to lung cancer.