Birnbaum et al. (10) first defined genes with “fetal effect,” and found that 25% of the more than 30,000 gene probes revealed transcript levels that were overexpressed or underexpressed in fetal life compared with the postnatal period. Then, they defined sets of risk genes that have been implicated as disease-predisposing for six neuropsychiatric disorders, including syndromic neurodevelopmental disorders, ASD, intellectual disability, schizophrenia, bipolar affective disorder, and neurodegenerative disorders. The authors then employed various statistical approaches as they explored the expression of these disease-predisposing gene sets in the BrainCloud data set. The outcome of this experiment was quite revealing: the authors observed increased fetal expression of disease-predisposing genes for syndromic neurodevelopmental disorders, intellectual disability, and ASD. In contrast, a statistically significant fetal underexpression of transcripts was reported for the gene set associated with neurodegenerative disorders. In a secondary analysis, the authors found that the ASD findings were a result of enrichment in transcripts originating from rare variants (CNVs) rather than the common variants (SNPs). Surprisingly, the group of schizophrenia or bipolar disease-predisposing genes (originating either from SNP, CNV, or exome sequencing studies) did not show enrichment in either direction. However, although the majority of schizophrenia susceptibility genes did not show fetal effects, these genes were still found to be important for neural development: gene ontology classification (12) revealed that they belonged to gene pathways related to “nervous system development” and “neuron differentiation.” Furthermore, within each CNV locus associated with schizophrenia, one or two genes were enriched in prenatal abundance, suggesting that they might be of particular relevance for disease-associated fetal pathogenesis.