If the loss or diminution of the daily peak in CNS dopaminergic activity rhythm is a primary signal to the clock circuit to drive its output control of metabolism towards metabolic syndrome, it is not surprising that a loss of singular signals (e.g., prolactin) in a redundant and subservient hierarchical organization of input signaling to the clock pacemaker circuit that are upstream from the dopaminergic input would be inconsequential to direct dopaminergic receptor replacement therapy for the metabolic syndrome. The gene discussed is CLOCK; the disease is metabolic syndrome.