Functionally, BICD2 has been reported to be localized in the Golgi complex and participates in membrane traffic from the Golgi apparatus toward the endoplasmic reticulum (ER) via a coat complex coatomer protein I (COPI)-independent pathway.34 In mice, the deficiency of BICD2 affects radial cerebellar migration of granule cells in the developing brain.35 In humans, coding mutations were also found in spinal muscular atrophy.36–38 In PBMCs, BICD2 is most abundant in naive B lymphocytes (supplementary figure S4). This evidence concerns the gene BICD2 and proximal spinal muscular atrophy.