Interestingly, Fang et al. found that, in gastric cancer, elevated OCT1 level facilitated canonical extracellular-signal-regulated kinase (ERK) signaling pathway by transactivating synbindin which binds to ERK DEF domain, resulting in activation of ERK substrates ELK1 and RSK which finally leads to increased proliferative capacity and metastatic competency [15]. This evidence concerns the gene ELK1 and gastric cancer.