We first engineered multiple clones of vector-matched PR-null T47D breast cancer cells expressing either WT PR-B or mutant K388R (KR) PR-B that is unable to undergo SUMO modification at Lys388; this SUMO-deficient receptor is a functional mimic for PR-B that is persistently phosphorylated on Ser294 [13,41]. This evidence concerns the gene RB1 and breast cancer.