reported that MLS occurrence and development depend on the Hippo/YAP1 pathway, and that the FUS-DDIT3-driven tyrosine-protein kinase receptor (IGF-IR)/PI3K/AKT signaling pathway promotes the stability and nuclear accumulation of YAP1 by “turning off” the Hippo signal. This evidence concerns the gene YAP1 and McLeod neuroacanthocytosis syndrome.