This hypothesis is based on the known fact that CNAs can sometimes provide oncogenic drivers, such as HER2 amplification in breast cancer26 and CCNE1 in ovarian cancer.27 In this study, we observed that silencing PKCι induced apoptosis in PRKCI-amplified ovarian cancer cells while it was well tolerated by cells without PRKCI amplification even though these lines displayed even greater abundance of PKCι (Figs. 3 and 4). The gene discussed is ERBB2; the disease is ovarian cancer.