In MLS, however, recurrent genetic alterations affecting Hippo pathway components have not been identified, pointing to a mechanism of nuclear YAP1 stabilization and activation that likely depends on FUS-DDIT3 and may involve oncogenic signaling cascades known to be active in MLS, such as the IGF-II/IGF-IR/PI3K/AKT axis [12–14]. The gene discussed is DDIT3; the disease is McLeod neuroacanthocytosis syndrome.