In Lee’s study, K63 linkage on LKB1 is enhanced by HRAS mutations, as the E3 ligase activity of Skp2 is greatly induced by HRAS mutations in HCC models.18 Whereas, our study focused on NSCLC, a different cancer type with a distinct cellular context harboring frequent KRAS mutations (30.9%);41 more importantly, the tumor suppressive function of LKB1 in NSCLC is well established and has been confirmed both in experimental models and NSCLC patients. The gene discussed is HRAS; the disease is neoplasm.