Tian et al. (2019) have found that ERas overexpression significantly increases the phosphorylation level of mTOR (Ser2448) and its substrate (ULK1-Ser757), as well as AKT-Ser473, activates the AKT/mTOR pathway, blocks autophagic flux in gastric cancer cells, suppresses DDP-induced apoptosis, and induces DDP resistance. In contrast, silencing ERas has been found to increase autophagic flux and enhance the sensitivity of gastric cancer cells to DDP in vitro (Tian et al., 2019). Here, MTOR is linked to gastric cancer.