Along the same line, we have shown that antiprogestin-responsive tumors from the murine MPA-induced breast cancer model had higher levels of PR isoform A (PRA) than PRB (Helguero et al. 2003), and when they acquired antiprogestin resistance there was a change in the PR isoform ratio toward B and thus a potential switch from mifepristone acting as an antagonist to an agonist (Helguero et al. 2003, Wargon et al. 2009, 2011, 2015). The gene discussed is RB1; the disease is breast carcinoma.