Two children with homozygous, likely null, mutations are microcephalic and severely encephalopathic (Shaheen et al., 2014); another child with a compound heterozygous mutation is also microcephalic and displays global developmental delay (Leduc et al., 2016) Thus, while MAGUKs such as PSD95 and SAP97 can substitute for each other in electrophysiological assays (Schlüter et al., 2006; Howard et al., 2010), our data indicate that CRIPT has a nonredundant and critical cell biological function in neurons. The gene discussed is DLG1; the disease is Global developmental delay.