This phenotype is very similar to that produced by loss of the anos1, which also encodes an FN3 superfamily member and is responsible for Kallmann syndrome, a condition that similarly presents with CHH and anosmia due to lack of proper GnRH and olfactory neuron migration (Stamou and Georgopoulos, 2018). Here, ANOS1 is linked to cartilage-hair hypoplasia.