Low-grade serous ovarian carcinomas (LGSOC) are associated with a poor response to chemotherapy and are largely characterised by RAS pathway activation. However, Ras-pathway activating mutations account for just over half of LGSC cases and there is an unmet need to identify other drugable targets for the non-ras mutated LGSC. Utilising whole-exome and targeted sequencing of the largest LGSOC cohort to date, we identified recurrent somatic mutations in cancer driver genes currently under investigation for their clinical utility, including the deubiquitinase USP9X (14%), along with KRAS (27%), BRAF (11%), NRAS (12%), EIF1AX (7%), NF1 (6%), NF2 (4%), MACF1 (8%), ASH1L (4%) and DOT1L (4%). Genome-wide copy number analysis identified low-level aberrations in LGSOC, with recurrent loss on chromosome arm 1p (38%) unique to LGSOC when compared to high-grade serous ovarian carcinomas. Immunohistochemistry further highlighted a subset of LGSOCs with either CDKN2A deletion (10%) or overexpression (6%). Currently, investigation is underway into the role that USP9X plays in the context of LGSOC; functional analysis of USP9X knockdown is being conducted using a panel of LGSOC patient-derived cell lines and analysis of USP9X knockout cell lines will be commencing soon. Proteomic and transcriptomic interrogation of USP9X knockdown/knockout is also being conducted in order to elucidate the pathway that the gene effects in LGSOC.Further study into genomic findings will help inform clinical decision-making of both Ras-pathway positive and negative LGSOC cases.