Collectively, these experimental observations suggest the possibility that alterations in the function of CDK12, and possibly CDK13, are implicated in axonopathies and neurodegenerative diseases, such as Alzheimer’s disease, for which the contribution of mechanisms regulated by these kinases (i.e., modulation of CDK5 expression [87–89], alterations of actin cytoskeleton remodelling [90] and heterochromatin status [87]) to the pathogenesis have been demonstrated. The gene discussed is CDK12; the disease is neurodegenerative disease.