DCX is phosphorylated by CDK5 on Ser297 residue (Tanaka et al., 2004), likewise on Ser47 by PKA and MARK (Schaar et al., 2004), both eventually led to reduction in DCX's binding affinity for MTs and in turn enhancing migration, a mechanism that can be implicated in the migration and invasion of highly invasive glioma (Figure 2). The gene discussed is DCX; the disease is glioma.