**1. Introduction**

Although the incidence of gastric cancer (GC) has declined steadily in recent years, GC remains a major cancer burden. GC is still the fifth most common malignancy and third leading cause of cancer death in both sexes worldwide, comprising 8.8% of total cancer deaths [1]. Radical resection is the only potentially curative approach for GC; however, approximately 40–70% of GC recurs even after curative resection [2]. When the disease reaches an

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advanced state, chemotherapy becomes a mainstay of the treatment [3]. The most frequently used first-line chemotherapy regimens worldwide are platinum derivatives plus fluoropyrimidine doublet or a triplet regimen with the addition of epirubicin or docetaxel. The reality is that chemotherapy has reached a plateau of efficacy for GC with a median overall survival (mOS) of around or less than 12 months [4, 5]. Furthermore, although second-line treatment is recommended for the patients with failure after first-line chemotherapy because it prolongs survival as compared with the best supportive care [6–8], the global standard regimens of second-line chemotherapy have not yet been determined [4].

These somewhat painfully slow rates of advances in treatment have been impetus to develop new concepts of strategies. As an example, receptor tyrosine kinases (RTKs) consist of the ligand binding of extracellular domains, a transmembrane domain, and a tyrosine kinase motif, which is involved in a subsequent downstream signal cascade. Since this cascade leads to cell growth, differentiation, adhesion, migration, and apoptosis [9], each step is theoretically a therapeutic target. This review focuses on advances in molecular targeted therapy for GC in recent years, as well as problems to be resolved.
