In addition, researchers in a recent study demonstrated that transgenic Met overexpression in the mouse mammary gland cooperates with conditional p53 loss to drive the formation of claudin-low mammary tumours, and they showed that claudin-low tumours developing in mice without the MMTV-Met transgene and only conditional mammary gland-specific deletion of p53 exhibited amplification of the endogenous Met gene [69]. The gene discussed is MET; the disease is breast cancer.