The ability of the overexpressed EphA2 to cause oncogenic transformation appears to be dependent on a low level of ligand-induced forward signalling, as the receptor is poorly tyrosine phosphorylated (see Section 9) in breast cancer cell lines, and ligand binding reversed the malignant phenotype of the cells conferred by EphA2 overexpression [9,50]. Here, EPHA2 is linked to breast cancer.