Endometriosis is an inflammatory disease defined by the presence of ectopic endometrial tissue outside the uterine cavity and is associated with infertility. An aberrant molecular phenotype of the eutopic endometrium in women with endometriosis is thought to affect endometrial receptivity. For successful maternal-embryonic dialog, an appropriate expression of growth factors, cytokines and hormones and their regulation of cell adhesion molecules is necessary. Many articles have found that certain biomarkers such as leukemia inhibiting factor (LIF) from the IL-6 family, glycodelin A (GdA) and αvβ3 integrin are abnormally downregulated in women with endometriosis. The altered expression of progesterone receptor expression also decreased expression of HOX genes in the eutopic endometrium, leading to an abnormal activation or repression of the downstream genes regulated by the HOX genes that produce biomarkers of endometrial receptivity. Understanding the molecular and cellular mechanisms of endometriosis-related reduction in uterine receptivity will guide future research for fertility treatment in women with endometriosis.