Amplification, mutation, or gene fusion of tyrosine kinases (TKs) constitutively hyperactivate the PI3K (phosphatidylinositol 3-kinase)/AKT (protein Kinase B) and RAS/extracellular signal-regulated kinase (ERK) pathways in many cancers [27,28,29], providing excellent opportunities for targeted cancer therapy. The gene discussed is CDC42; the disease is cancer.