The decrease in the nuclear pool of Smurf2 would diminish its ability to negatively regulate the pro-tumorigenic factors residing in the nucleus, while increased Smurf2 abundance in the cytoplasm would facilitate the cancer-promoting pathways, including EGFR-induced and KRAS-mediated signaling pathways and, suggestively, the WNT/β-CATENIN pathway [18]. The gene discussed is KRAS; the disease is cancer.