Consistently, experiments performed in mouse mammary epithelial cells (MMECs) overexpressing p130Cas demonstrate that p130Cas expression leads to hyperactivation of the tyrosine kinase receptor c-Kit, indicating that high levels of p130Cas, via abnormal c-Kit activation, promote mammary luminal cell plasticity, thus providing the conditions for the development of basal-like breast cancer (Figure 2C; Tornillo et al., 2013). The gene discussed is KIT; the disease is breast carcinoma.