Prevention of psychosis is a key goal, given the severity and functional impact of psychotic disorders.1,2 Research has established reliable criteria to identify people considered at clinical or ultrahigh risk for psychosis. Naturalistic studies yield conversion rates to psychosis of 17.7% at 6 months, 21.7% at 12 months, and up to 31.5% over 3 years.3 However, conversion rates to psychosis have declined in recent years,3 challenging prevention trials. Nevertheless, with data pooled,4 efficacy has been established in randomized clinical trials for cognitive behavioral therapy, antipsychotics and, long-chain ω-3 polyunsaturated fatty acids (ω-3 PUFAs). Although ω-3 PUFA treatment is attractive for prevention from a pathophysiologic perspective and because of its benign adverse effect profile, preventive efficacy of ω-3 PUFAs for psychosis had been demonstrated in only 1 single-site study (N = 81).5 Only 3 months of ω-3 PUFA treatment led to a significant reduction in transition to psychosis both at the end of active treatment and 9 months after discontinuation (ω-3 PUFA, 4.9% vs placebo, 27.5%), translating into a number needed to treat (NNT) of 4. This finding persisted in the naturalistic, long-term follow-up (median duration, 6.7 years6), clearly calling for replication.