These studies reinforce the specificity of action of DLX3 and GCM1 on PGF (compared to the CGA reporter) and further suggest that the mechanisms leading to the TDO phenotype in humans are clearly separable from the impact of DLX3 transactivation potential of genes like CGA and PGF and the functional antagonism between DLX3 and GCM1. The gene discussed is GCM1; the disease is tricho-dento-osseous syndrome.