Specifically, MCR signaling potentiates CNS-restricted NA release from locus ceruleus (LC) nerve endings.29 MCR signaling also increases tyrosine hydroxylase mRNA and, hence, NA synthesis within the LC.29 Released NA, bound to β2-adrenegic receptors on microglia, promotes microglial quiescence.12 To the contrary, LC ablation causes NA depletion throughout the cortex and frees microglia to make proinflammatory cytokines.30 Ultimately, decreased LC metabolism in MS links to cognitive impairment.31 Here, NR3C2 is linked to myeloid sarcoma.