Serine–threonine kinases target phosphorylation sites through the chemical properties of flanking amino acid sequences, but will phosphorylate suboptimal sites, particularly when competition from other kinases is low and additional specificity factors are lacking.14 One hypothesis could be that changes in activity or specificity of AKT or JNK in schizophrenia allow other kinases to compete at sequences normally optimal for AKT or JNK. Here, AKT1 is linked to schizophrenia.