The current limited utility of PRS should not be taken to imply that there is no future for precision medicine in psychiatry. For some disorders, such as Autism Spectrum Disorders, highly penetrant mutations, copy number variants and chromosomal rearrangements have been compiled into genetic panels used for prediction (Vorstman et al., 2017). Even for other disorders, certain monogenic origins are routinely ruled out in clinical practice (e.g., a deletion on chromosome 22q that causes a schizophrenia-like syndrome) (Bassett and Chow, 2008). To improve and begin to personalize treatments, particularly for the broader range of psychiatric disorders characterized by such polygenicity and largely unknown mechanisms, it may be important to not rely on markers of genomic risk for disorder expression (which may usefully identify new therapeutic targets), but rather on markers of response to current treatments. Consistent with this speculation, one recent approach found no associations between depression and SCZ PRS and response to antidepressants (Garcia-Gonzalez et al., 2017) among 3756 treatment receiving patients. Further, pharmacogenomics GWAS (i.e., the study of treatment response) have consistently revealed larger effects (OR 2.5) than
