Interpreting the XPD mutations in the context of available biochemical and epidemiologic data led us to propose that specific subset of XPD mutations in the fetus, associated with TTD but not XP, may result in higher risk of preeclampsia due to their adverse effects on binding of XPD with the CAK and p44 subunits of TFIIH, leading to impairment of TFIIH-mediated functions in placenta [18]. The gene discussed is ERCC2; the disease is preeclampsia.