In a previous study, Dragin et al. (2006) reported that maternal hepatic CYP1A2 and maternal hepatic human CYP1A2 (in place of the mouse analogous protein) provided protection from TCDD-induced cleft palate and hydronephrosis, and that absence of maternal CYP1A2 increased sensitivity to TCDD-induced birth defects. Here, CYP1A2 is linked to hydronephrosis.