FTO restrains HOXB13 methylation, and the overexpression of FTO and HOXB13 drives GC cell proliferation, migration, and invasion through PI3K/AKT/mTOR signaling via IGF-1R.[121] Moreover, FTO demethylates caveolin-1 mRNA, enhances its degradation, regulates mitochondrial metabolism, and promotes cell proliferation and metastasis in GC.[124] Yue et al. suggested that a positive feedforward loop between ALKBH5 and NF-κB signaling associated with m6A modification generates the intestinal metaplasia phenotype of gastric epithelial cells.[125]. This evidence concerns the gene IGF1R and gastric cancer.