A CNS functional interaction between COMT and PRODH has been proposed by Paterlini et al., who suggested that significant cortical Comt upregulation in the Prodh-null mouse represents a compensatory response to increased PFC dopamine transmission, arising as a consequence of PRODH deficiency enhancing glutamatergic synaptic transmission.8 In addition, psychosis with positive symptoms,20 decreased smooth pursuit eye movement,27 and deficits in visual processing,28 have been associated with high levels of plasma proline in 22q11DS patients carrying the low-activity Met allele. Here, PRODH is linked to 22q11.2 deletion syndrome.