Mechanistically, patients harboring isoform BRAF3-9 (Δ exons 4–8) or BRAF2-6 (Δ exons 3–5) that could eliminate RAS-binding domains often develop drug resistance.27,28 Advanced prostate cancer is commonly treated with drugs that inhibit androgen biosynthesis or antagonize the interaction between androgen and androgen receptor (AR). This evidence concerns the gene AR and prostate carcinoma.