Whilst other rare types of ovarian neoplasms have been found to be underpinned by highly recurrent mutations, such as FOXL2 hotspot mutations in adult-type granulosa cell tumors9 or SMARCA4 loss-of-function mutations in small cell carcinomas of the ovary hypercalcemic type12, SSTs were found to be characterized by recurrent and likely pathognomonic FHL2-GLI2 fusion genes. Here, FHL2 is linked to ovarian neoplasm.