DPYSL2 and HIV-associated neurocognitive disorder: The present study suggests that hyperphosphorylation of CRMP2 may be an important feature of HIV-associated neurodegeneration, and identifies a potential link between abnormal activation of CDK5 and impaired neurogenesis that has been observed in animal models of HIV neurotoxicity [36], however future studies will be necessary to elucidate whether CRMP2 hyperphosphorylation plays a direct causative role in neurogenic or neurodegenerative alterations in the pathogenesis of HAND.