In studies on esophageal adenocarcinoma, the antiproliferative effect of protoanthocyanidins was observed, showing their ability to stop the cell cycle, induce apoptosis, or trigger autophagy as an alternative mechanism involving PI3K (phosphoinositide-3-kinase), AKT (Protein kinase B) and the mammalian target of rapamycin (mTOR) signaling [131]. This evidence concerns the gene MTOR and esophageal adenocarcinoma.