These studies have revealed that constitutively activating and kinase-dead mutations could play context-dependent opposing roles in cancer and may be simultaneously present in a variety of oncogenic kinases such as FGFR2/FGFR3 [64–68], MAP2 K4 [69], EPHA3 [70], DAPK3 [71], TRKB [72], ITK [73], and LKB1 [74]. The gene discussed is EPHA3; the disease is cancer.