The limited function of HER3 and trastuzumab resistance in GC can be attributed to the facts that HER2 has no ligand and HER3’s intrinsic tyrosine kinase domain is defective, HER3 usually heterodimerizes with HER2, and the HER2/HER3 heterodimer is likely to be the most effective complex of all the heterodimers [46–47]. The gene discussed is ERBB2; the disease is gastric cancer.