Initially, RASAL2 was identified as a potential RAS GAP tumor suppressor in a functional cell-based screen.25 McLaughlin et al.18 further demonstrated that RASAL2 appeared to be more frequently silenced by epigenetic mechanisms in breast cancer, and RASAL2 suppression promoted breast tumor development as a consequence of activating K- and H-RAS based on the studies with human xenografts and genetically engineered mouse models. Here, HRAS is linked to breast carcinoma.