High expression of FTO maintains the stability of resistance genes (such as MYC and β-catenin) through demethylation, leading to resistance to tyrosine kinase inhibitors (TKIs) and PARP inhibitors (Yan et al., 2018; Fukumoto et al., 2019); conversely, inhibiting METTL3 or FTO can reverse resistance and enhance sensitivity to targeted drugs and immunotherapy, making both key targets for overcoming targeted resistance in GC (Cui Y. H. et al., 2024). Here, PARP1 is linked to gastric cancer.