As shown in Figure 1A, there was an increased expression of PRC2 complex proteins such as EED (0.0067), as well as a noticeable trend in overexpression of corresponding genes in ectopic tissues from endometriosis patients, particularly in EZH2. This correlates with the findings of Colon-Caraballo and colleagues [8,23] and supports the characterization of EZH2 as a contributor to transcriptional repression and progression of the disease. Here, EED is linked to endometriosis.