A study focusing on the natural anti-metastatic agent antrocin has shown that it could act as an EMT inhibitor, restoring E-cadherin protein levels in parallel with the increase in DR5 expression,84 whereas another study has shown that DR5 knockdown could increase E-cadherin expression and diminish migration in breast cancer, which further suggests a specific regulatory step.85 However, how DR4/DR5 and E-cadherin expression is simultaneously regulated is still not well understood. The gene discussed is CDH1; the disease is breast cancer.