One class of resistant prostate tumors continues to rely upon androgen receptor (AR) signaling through a number of means, including: over-expression of the AR gene, through DNA amplification or some other mechanism [14,23]; "promiscuous" point mutation in AR, allowing the receptor to be activated by steroids other than androgen, including anti-androgens and estrogen [24]; and ligand-independent activation of AR, mediated by oncogenes such as ERBB2 or HRAS [25]. Here, HRAS is linked to prostate neoplasm.