The migration defect could potentially explain ARCND features through a reduction in NCC reaching the first and second pharyngeal arches, resulting in malformed derivatives such as mandible and external ear, a mechanism that also seems to be involved in RCPS.17 In regard to HDAC9, even though its overexpression has been associated with increased proliferation and migration in cancer cells, to date this gene has not been associated with neural crest proliferation/migration or specification of craniofacial elements. Here, SLC12A3 is linked to cancer.