RHOA and gastric cancer: Meanwhile, gastric cancer cells with ras homolog family member A (RHOA) Y42 mutation produced free fatty acids in the microenvironment through phosphoinositide-3-kinase (PI3K)/PKB/mammalian target of rapamycin (mTOR) signaling, which also enhanced the immunosuppressive function of Tregs and promoted their aggregation in the low-glucose tumor microenvironment [57].