However, the impact of estradiol which further increased the development of endometriosis-like lesions predominantly demonstrated the requirement of ERα for cell adhesion and proliferation, and for the neoangiogenesis that supports endometriosis-like lesion growth because the impact of an ERβ gene knockout was less than ERα gene deletion in the suppression of ectopic lesion growth [51]. Here, ESR2 is linked to endometriosis.