An alternative mechanism of proliferation-promoting action by PTHrP (1–34) has been proposed by DaSilva and coworkers [46] who demonstrated that under low androgen concentration LNCaP prostate cancer cells exposed to PTHrP up-regulate the androgen receptor (AR) via epidermal growth factor receptor and Src kinase activation-controlled restraining of proteosomal AR degradation. This evidence concerns the gene AR and prostate carcinoma.