RAMP1 is an accessory protein that modulates G-protein coupled receptor signaling, functioning as a critical co-receptor required for transport of CALCRL to the plasma membrane and formation of receptor complexes with calcitonin gene-related peptide (CGRP) and amylin. Beyond its canonical role in neuropeptide signaling, RAMP1 mediates neuro-immune communication with broad pathological consequences. CGRP-RAMP1 signaling on immune cells suppresses anti-tumor CD8+ T cell responses in melanoma 1, while promoting tissue repair through enhanced macrophage efferocytosis and polarization following acute injury 2. In cancer contexts, sensory neuron-derived CGRP acts via RAMP1 on cancer-associated fibroblasts to drive collagen deposition and immune exclusion in triple-negative breast cancer 3, and on cancer cells directly to promote gastric tumor growth and metastasis 4. RAMP1 on intestinal goblet cells mediates CGRP-driven mucus secretion essential for gut barrier protection 5, while RAMP1 on meningeal macrophages facilitates bacterial invasion by suppressing antimicrobial immunity 6. In endometriosis, CGRP-RAMP1 signaling on macrophages drives lesion growth and pain, and FDA-approved CGRP-blocking agents reduce both measures 7. These findings establish RAMP1 as a therapeutic target with approved drugs including zavegepant and pramlintide available for clinical development.