Furthermore, anti-CNTN1 autoantibodies can cause reduction in contactin-1 surface expression on dorsal root ganglionic and cerebellar neurons and decrease the sodium currents in the dorsal root ganglionic cells without affecting the sodium channel density, providing a pathophysiologic correlate of sensory ataxia often seen in these patients [21]; the antibody subclass in this study was not however specified. The gene discussed is CNTN1; the disease is sensory ataxia.