For example, in the genetic screen performed by Guo and colleagues, silencing of the Bardet-Biedl Syndrome-associated BBS7 gene led to a disrupted apical-basal polarity of radial glial cells, but also to a defective multipolar to bipolar transition of migrating principal neurons, and to altered axonal trajectory and fasciculation of cortical neurons (Guo et al., 2015). This evidence concerns the gene BBS7 and Bardet-Biedl syndrome.