To date, there have been few publications exploring the pathogenicity of mutant FOXL2. The transactivation capability of mutant FOXL2 on known wildtype FOXL2 targets has been investigated, whilst one report describes the inability of mutant FOXL2 to elicit an effective apoptotic signalling cascade to be partially accountable for the pathophysiology of GCT development [18], [20]. This evidence concerns the gene FOXL2 and granular cell tumor.