To understand how Trappc9 deficiency may cause microcephaly, we first looked at embryonic neurogenesis in zebrafish using whole mount in situ hybridization (WISH) to examine the changes in neural stem cells (NSCs) and neural progenitor cells (NPCs) with the well-established marker sox2. There was no significant difference in sox2 expression patterns or levels between zTrappc9 mutant, zTrappc9 morphant, and wildtype embryos at 24 hpf, 48 hpf (data not shown), or 72 hpf (Figure S4A, B). The gene discussed is SOX2; the disease is microcephaly.