Mutations in ARID1A (at-rich interaction domain-containing protein 1A), a tumor-suppressor gene, and loss of the ARID1A-encoded protein, BAF250a, are evident in 46% of CCCs, 30% of endometrioid cancers, and many contiguous atypical endometriosis, but these changes are not observed in high-grade serous ovarian carcinoma [20,21]; these differences explain, at least in part, how these somatic mutations may trigger transformation of endometriosis into CCC or endometrioid carcinoma. This evidence concerns the gene ARID1A and endometriosis.