The two lentivirally infected cancer cell lines, which do not express detectable endogenous EphA3 or ephrin-A3 (Figure 1), were then treated with ephrin-A3 Fc (a soluble form of the ephrin-A3 ligand fused to the Fc portion of human IgG1) to activate EphA3 through ephrin binding in trans. Ephrin-A3 Fc increased receptor tyrosine phosphorylation in the cells coexpressing EphA3 with control mCherry, as expected, but not in the cells coexpressing EphA3 with mCherry-ephrin-A3 (Figure 1A,B). This evidence concerns the gene EPHA3 and cancer.