The former include (i) sustained androgen receptor (AR) signaling due to overexpression of AR, coactivator of the AR or androgen production inside the prostate tumor; (ii) activation of tyrosine kinase receptor IGFR-1, EGFR, VEGFR and downstream signal transduction pathways like PI3K/AKT and Ras/Raf/MEK/ERK pathways; (iii) aberrant angiogenesis, (iv) stroma-derived cytokines and growth factors which promote cell growth and resistance to chemotherapy. This evidence concerns the gene AR and prostate neoplasm.