A tumor-suppressive role of EPHA3, in particular for lung cancer, is supported by the reduction in receptor activity conferred by the point mutations found in cancers, and ligand- and EPHA3-dependent apoptosis of tumor and stroma cells upon receptor agonist treatment, suggesting that wild-type EPHA3 has anti-tumorigenic properties (Lahtela et al., 2013; Lisabeth et al., 2012; Vail et al., 2014; Zhuang et al., 2012). This evidence concerns the gene EPHA3 and lung cancer.