In addition, rapid or nongenomic PR effects in breast cancer have been described in several works, including ours, demonstrating[2] PR ability to activate c-Src, p42/p44 mitogen-activated protein kinases (MAPKs)[3-5], phosphatidylinositol 3-kinase (PI-3 K)/Akt[5], and Jaks/signal transducer and activator of transcription 3 (Stat3)[6,7] pathways, which in turn mediate multiple aspects of PR function[1,8]. The gene discussed is PGR; the disease is breast cancer.