Inspired by the idiopathic pain reported by patients with Neurofibromatosis type 1 (NF1), we found that deleting the Nf1 gene (coding for the protein neurofibromin) using clustered regularly interspaced short palindromic repeats and CRISPR-associated (Cas9) (CRISPR/Cas9) in DRG could elicit hyperalgesic behaviors [4–6]. Here, NF1 is linked to neurofibromatosis type 1.