Given that Grb2 is naturally overexpressed in whole brain lysates of AD patients and also that it sequesters AICD in vesicles (McShea et al., 1999; Raychaudhuri and Mukhopadhyay, 2010; Roy et al., 2014), it was reasonable to hypothesize that Grb2 might reverse the cytoskeletal protein degradation in AD-like conditions. The gene discussed is DNM2; the disease is Alzheimer disease.