Hormonal levels (i.e., endogenous versus exogenous high levels), tissue placement (i.e., subcuticular versus intraperitoneal), and genetic changes important to endometriosis-associated ovarian cancers (i.e., oncogenic KRAS, loss of function ARID1A) must be considered when using these menstrual endometriosis models. This evidence concerns the gene ARID1A and ovarian carcinoma.