Additionally, the analysis is limited to gene level associations with disease and does not account for disorder/disease-associated differences in expression levels, post-translational modifications or protein-targeting pathophysiological mechanisms, like autoantibody production, all of which have been described for CRMP2 (e.g., changes in protein expression levels in several neurological conditions [125], hyperphosphorylation in Alzheimer’s disease [126–128], and auto-antibodies in autism spectrum disorders [129]). Here, DPYSL2 is linked to early-onset autosomal dominant Alzheimer disease.