Furthermore, we show that, similar to the other estrogen-dependent phenotypic changes in HSD17B1TG mice [16,19,20], the adenomyosis phenotype was prevented by the treatment with HSD17B1 inhibitor, confirming the dependence of the phenotype on the action of HSD17B1 and suggesting that increased estrogen exposure is upstream of all the altered adenomyosis-associated pathways. Here, HSD17B1 is linked to adenomyosis.