These include the loss or downregulation of PD‐L1 expression on tumor cells, the emergence of mutations in IFN signaling pathway components (e.g., Janus Kinase 1/2 mutations) which impair antigen presentation machinery and T cell effector functions, or the upregulation of alternative immune checkpoints leading to persistent T cell exhaustion [13, 14]. Here, CD274 is linked to neoplasm.