These findings suggest that endometriosis-derived organoids could respond differently to hormones due to altered expression of genes like PGR, ESR1, HSD11B1, LIFR, and PRLR alongside pathways (PI3K-AKT, WNT) that amplify the hormonal effects, making it a valuable model to study endometriosis (101). This evidence concerns the gene PRLR and endometriosis.