Just as UGT and transporter distributions can determine the therapeutic effectiveness of drugs metabolized by the glucuronidation pathway [66,67,87], the same process can also lead to endocrine environments favoring disease development (ASD, ADHD, PCOS, PD, and AD), with the actual disease being a function of a particular endocrine environment. The gene discussed is SLC35A2; the disease is attention deficit-hyperactivity disorder.