Moreover, and as a further demonstration that indeed the transcriptional effects of Stat3, PR and ErbB-2 govern cyclin D1 expression and in vivo progestin-induced breast cancer growth, comparable Stat3 phosphorylation levels and ErbB-2 phosphorylation at one of the major sites of autophosphorylation, Tyr 1272, as well as at Tyr 877, a site other than the autophosphorylation ones, which we already revealed is rapidly phosphorylated by progestins[9], were detected in all tumors (Figure 6G). The gene discussed is STAT3; the disease is breast cancer.