We hypothesize that overexpressed B7-H4 in adenomyosis participates in the formation of an immunotolerant environment of the uterus by negatively regulating T cell proliferation, facilitating immune evasion of ectopic endometrial lesions, preventing the effective elimination of lesions and leading to the development of uterine adenomyosis. This evidence concerns the gene VTCN1 and adenomyosis.