In C57/BL6 cortical neurons, the pharmacological inhibition of Pin1 catalytic activity with PiB (diethyl-1,3,6,8-tetrahydro-1,3,6,8-tetraoxobenzol-phenanthroline-2,7-diacetate) or Pin1 siRNA-mediated knockout induced an increase in ubiquitin-regulated modification of PSD proteins and a reduction in Shank3 protein levels [12], an observation consistent with Shank3 protein loss and enhanced ubiquitination described in AD brains [44, 45]. Here, PIN1 is linked to Alzheimer disease.