Because ligand-dependent EphA2 receptor signaling has been associated with tumor suppression whereas EphA2 ligand-independent signaling promotes tumor initiation and malignancy in breast cancer [44], [45], it is tempting to speculate that the secreted MSP domain may compete with ligand for binding to EphA2 receptor, thereby blocking EphA2-tumor suppressive function. The gene discussed is EPHA2; the disease is breast carcinoma.