Although the precise nature of NF1-linked pain syndromes remains unknown, patients clearly experience pain independent of their tumor burden, and these findings affirm the necessity of CRMP2 in NF1-related pain, while suggesting a physiological role for neurofibromin’s C-terminal domain-mediated inhibition of the CRMP2–Cav2.2 interaction [106]. The gene discussed is DPYSL2; the disease is neoplasm.