Recently, a 2018 paper by Hung and colleagues demonstrated that an antibody directed to the N192 and N200 glycosylation sites of PD-L1 (STM108) inhibited PD-L1 interactions with PD-1, and led to PD-L1 internalization and degradation; moreover, when the antibody was conjugated to an anti-mitotic drug, it reduced tumor growth in an animal model system using mouse breast cancer cells [21]. The gene discussed is CD274; the disease is neoplasm.