We are wary that our study possesses some limits; firstly, its retrospective nature, which does not allow to draw conclusions about cause–effect relationships; secondarily, for Multiple Sclerosis, no CSF markers of axonal loss or of immunophenotype were measured, thus, not allowing us to assess a relationship between CGRP content and neuroaxonal loss or specific inflammatory immunophenotypes. This evidence concerns the gene CALCA and multiple sclerosis.