High levels of ErbB2 in cancer cells induce ligand-independent constitutive dimerization of ErbB2 and/or dimerization with other epidermal growth factor receptor family members, triggering downstream signaling through the phosphoinositide-3-kinase (PI3K)–AKT and Ras–Raf–MEK–ERK1/2 cascades [3]. The gene discussed is AKT1; the disease is cancer.