Supporting a conserved role of SUMOylation in silencing of the MHC-I/APM pathway, pharmacological inhibition of SUMOylation significantly amplified the IFN-γ–dependent induction of MHC-I levels in osteosarcoma, neuroblastoma, breast cancer, and lung cancer cells (Figure 5G and Supplemental Figure 6C). The gene discussed is IFNG; the disease is lung cancer.