It is well established that the Phosphoinositide-3-Kinase (PI3K)/v-AKT Murine Thymoma Viral Oncogene Homolog 1 (AKT) pathway is frequently dysregulated in cancer.4, 5, 6 By activation of AKT and other downstream effectors, the PI3K pathway regulates a broad spectrum of processes essential for cancer, including cell survival, proliferation, growth, metabolism and angiogenesis.6, 7, 8 The PI3K pathway can be activated by genetic alterations in PIK3CA, TSC1/2, LKB1 and Pten, or by the activation of upstream inducers such as IGF and HGF/c-Met signaling. The gene discussed is MET; the disease is cancer.