How might this be explained with the observations of the direct (Egan et al., 2011; Kim et al., 2011) and indirect (Hardie, 2008, 2011b) activation of autophagy by AMPK and the attenuated tauopathy reported in different models after autophagy induction (Congdon et al., 2012; Schaeffer et al., 2012)? The gene discussed is PRKAA1; the disease is tauopathy.