Reproductive tissues respond to steroid hormones and thus are particularly vulnerable to the effects of exogenous steroid 'mimic' compounds (endocrine disrupters). One such endocrine disrupter, diethylstilbestrol (DES), is linked to gynecological cancers and changes in uterine structure that reduce or completely abrogate reproductive competence. Until recently, little was known about the identity of target genes and signaling pathways involved in pathologies linked to endocrine disrupters such as DES. We outline genetic, cellular and molecular roles for patterning genes, with emphasis on homeobox and Wnt genes. There is evidence that changes in the expression of Wnt and homeogenes underlie many of the defects induced by DES. Data obtained from murine systems will likely apply to a broad spectrum of gynecological pathologies involving abnormal cell behaviors ranging from fibroids to malignant tumors. Knowledge garnered from modern molecular genetics should lead to progress in the emerging field of molecular gynecology.