Nodal, a member of the TGF-B superfamily of growth factors, controls visceral organ Left-Right (LR) asymmetry in vertebrates as well as some epithalamic brain LR asymmetries that exist in zebrafish but are not apparent in mammals. But the pathways that operate broadly in all vertebrates to establish brain Left-Right asymmetry and lateralized behaviors are unknown. At least some of these unknown pathways are thought to be Nodal-independent, since lateralized behaviors like handedness and right ear hearing advantage are normal in human patients with Left-Right reversed Nodal signaling. We present evidence that the Rere protein is part of a Nodal-independent pathway needed for zebrafish brain laterality. Rere is a nuclear receptor co-regulator required for optimal Retinoic Acid signaling as well as for modulating other pathways. In humans, RERE is a candidate risk gene for schizophrenia and autism spectrum disorders. We find that heterozygosity for the rerea mutation, babtb210, disrupts normal population-level laterality of adult zebrafish females without disrupting other behavioral parameters and without perturbing nodal (southpaw) expression and function. We compare these results to the results for population-level laterality of adult zebrafish males heterozygous for the babtb210 allele. We also examine the role of rerea and other factors in establishing and/or maintaining bilateral symmetry in the zebrafish embryo. Finally, we discuss the relevance of our results for human-specific traits like handedness and language, as well as the implications for human congenital diseases and neurodevelopmental disorders like schizophrenia and autism, which often have disruptions of bilateral symmetry and/or of LR asymmetry.