ARID1A and neoplasm: These anatomically distinct tumors have overlapping gene expression profiles and possess similar mutational landscapes, with frequent variants in ARID1A (around 50% of CCOC), PIK3CA, and PTEN, which supports treating them together as a single histopathological entity.4,11,12,13,14,15 CCGC have an immune-rich tumor microenvironment contributed to by various mechanisms, including mismatch repair (MMR) deficiency, estimated at 5% to 10% of CCOC, frequent ARID1A variants, and upregulation of IL-6 and other pro-inflammatory cytokine signaling.