Functional exploration of autophagy repression in UBE2C-drived lung carcinogenesis not only revealed that autophagy inhibitors BA1 or 3-MA dose-dependently blocked UBE2C deficiency-induced cellular proliferation arrest of A549 and H1299 cells respectively in our proliferation assay (Fig. 5b), but also indicated that BA1 or 3-MA treatments blocked elevation of pro-apoptosis protein caspase-3 induced by UBE2C downregulation and decreased UBE2C knockdown-induced apoptosis and senescence in A549 cells respectively (Fig. 5c, d; Supplementary Figure S1E and G). Here, CASP3 is linked to medical procedure.