Where do we go from here? Improving infant brain inhibition is not prevention of schizophrenia. A surrogate marker is probably the only option for studying prevention of a disorder that will not occur for decades. The folic acid/neural tube defect studies had the research advantage of a disorder manifest early in life. Is it possible to carry out a large preventive study where the clinical outcome will not be known for so long? One hope is that neurodevelopmental improvement would be nonspecific and that choline treatment could improve multiple behaviors, such as attention (already suggested by the authors’ data on 4-year-olds with poor inhibition in infancy), impulsivity, or mood instability, all of which could be measured long before the age of risk for psychosis. Even if such a treatment were effective, the many known risk factors for schizophrenia would mean that addressing any one of them might not make a significant difference in long-term outcome. For example, in a recent study genetic risk factors even in multiplex families accounted for only 0.4% of the risk for illness (7). At the other extreme, prevention of 44% of the cases of schizophrenia has been postulated through neonatal vitamin D supplementation for a particular Danish cohort of cases (8). It is probable that risk varies widely with time period and populations (9). Prenatal exposures to infection and malnutrition are the best bets for public health intervention, but a clear way forward is not yet compelling.