The somatic mutational landscape of this tumor has been well described, with a nearly pathognomonic FOXL2 p.C134W mutation in 85%–95% of cases, as well as less frequent recurrent TERT promoter (~40%), KMT2D (~17%), CDH1 (~9%), and TP53 (~5%) mutations.1, 2, 3. This evidence concerns the gene FOXL2 and neoplasm.