Drug resistance in tumor cells could occur through several mechanisms, including disabling mutations in Janus kinase 1 (JAK1), JAK2, and beta 2-microglobulin (B2M) genes; PD-L1 upregulation; decreased major histocompatibility complex (MHC) expression; increased PD-L2 levels on PD-L1 negative cancer cells; stromal remodeling; epithelial–mesenchymal transition (EMT); and host cells (including T cells) expressing PD-L1 [101]. The gene discussed is PDCD1LG2; the disease is neoplasm.