The paths between bicalutamide and prostate cancer point to several downstream targets of this drug, including the epigenetic regulator KMT2D, which is known to sustain prostate carcinogenesis by epigenetic mechanisms [37], and NECAB3, known to enhance the activity of HIF1A, thus promoting glycolysis under normoxic conditions and enhancing tumorigenicity in cancer cells [38]. This evidence concerns the gene HIF1A and medical procedure.