For genes such as Cul3 for which neuronal function remains underexplored, homozygous deletion is among the best tools to elucidate function, particularly for autism risk genes (Blundell et al., 2009; Etherton et al., 2009; Zhou et al., 2009; Blundell et al., 2010; Espinosa et al., 2015; Escamilla et al., 2017; Jaramillo et al., 2017). This evidence concerns the gene CUL3 and autism.