These findings not only provide a new inhibitor against DUB(s) with the potential to be developed as a candidate compound for cancer therapy, but also implicated that the pharmacological inhibition of JOSD2 by small molecular compound(s) could reactivate LKB1 by modulating its K6 linkage, thus further verified this newly-established JOSD2-LKB1 axis which was critical for NSCLC proliferation. The gene discussed is JOSD2; the disease is cancer.