In this study, we showed in DLB parietal cortex a specific increase of CRMP2 phosphorylation at Thr514 (Fig. 1), which is known to reduce CRMP2 binding affinity to molecules involved in axonal growth and microtubule dynamics, thereby inhibiting axonal function and leading to axonal pathology [6, 41–44]. The gene discussed is DPYSL2; the disease is Lewy body dementia.