The low level of exenatide detected in the CSF may not accurately reflect neuroparenchymal levels, although evidence from a previous exenatide trial in PD suggests this level of central nervous system (CNS) penetration was sufficient to engage neuronal insulin resistance pathways,12 but casts doubt whether this agent can sufficiently engage neuronal or glial GLP‐1 receptors that are theoretically necessary. Here, INS is linked to Parkinson disease.