Studies with breast cancer cells have also demonstrated key differences in the interactions of estrogen receptors with TP53: ERα recruits SUV39H1/H2 to induce histone H3 lysine 9 trimethylation to silence TP53-activated transcription, an effect that is opposed by ERβ, which induces activating heterochromatin conformation by inducing histone H3 lysine 4 trimethylation and RNA polymerase II recruitment to ERα-repressed TP53-activated genes (81). The gene discussed is TP53; the disease is breast cancer.