TEAD1 and gastric cancer: In conclusion, our findings provide evidence that ACAT2 plays a significant role in promoting the proliferation and metastasis of GC cells in vivo and in vitro, and the molecular mechanisms underlying this phenotype are that the downstream gene SETD7 of ACAT2 methylates YAP1 and suppresses its ubiquitination and degradation, activating the YAP1/TAZ-TEAD1 axis that contributes to GC cell malignancy.