Previous work by us and others have described and identified that growth hormone (GH) action drives several molecular mechanisms of anticancer therapy resistance, including upregulation of ATP-binding cassettes (ABC) containing multidrug transporter expressions and epithelial-to-mesenchymal transition (EMT) transcription factors in multiple cancer types (liver, bladder, pancreas, breast, colon, endometrium, and prostate cancer) that express the GH receptor (GHR) [7,8,9,10,11,12,13,14]. This evidence concerns the gene GH1 and prostate carcinoma.