Moreover, endometriosis-derived organoids appear to recapitulate and retain the endometriosis-linked attenuated responsiveness to progesterone (such as the reduced expression response of the target genes 17β-hydroxysteroid dehydrogenase 2 (17HSDβ2), PAEP, SPP1 and LIF), as well as tissue-reproducing epigenetic changes (in particular, hypermethylation of the PR promoter leading to decreased expression of the longer isoform PR-B, and methylation changes in HOX cluster genes) [140,141]. This evidence concerns the gene PGR and endometriosis.