The receptor tyrosine kinase (RTK) submodel, inspired by several prior models [22,23], depicts ligand-binding and dimerization reactions for many receptors that are frequently overexpressed, mutated or implicated in cancer, including the ErbB family (HER1-4), the hepatocyte growth factor receptor (cMet), the platelet-derived growth factor receptor (PDGFR), the fibroblast growth factor receptor (FGFR), the insulin-like growth factor receptor (IGFR), and the insulin receptor (INSR). This evidence concerns the gene PDGFRB and cancer.