SHC1 and neurodegenerative disease: Consistent with this model, our previous work has demonstrated a key role for p66-generated stresses in the propagation of neurodegenerative disease; genetic inactivation of p66 reduced the extent of axonal damage in spinal cords and optic nerves following EAE induction (Su et al., 2012) as did elimination of CyPD (Forte et al., 2007), establishing a functional interaction between p66 and the PTP on an in vivo level.