Genetically, the vast majority of MLS are characterized by a t(12;16)(q13;p11) chromosomal translocation that juxtaposes parts of the FUS gene to the entire coding sequence of DDIT3. The resulting FUS‐DDIT3 fusion protein, which acts as a transcriptional (dys‐)regulator, has been shown to play an essential role in MLS pathogenesis (Kuroda et al, 1997; Perez‐Losada et al, 2000; Engstrom et al, 2006; Riggi et al, 2006), but its mode of action remains incompletely understood. The gene discussed is FUS; the disease is McLeod neuroacanthocytosis syndrome.