Indeed in our study, cancer-promoting attributes such as cell survival, anchorage independent growth and invasiveness, which are supported by HBx, suffered a major setback when cellular levels of SIRT7 were depleted either using RNAi or inhibition of DUB activity, arguing for a strong role of SIRT7 in furthering the oncogenic program set in by HBx. The gene discussed is SIRT7; the disease is cancer.