Programmed death ligand 1 (PD-L1, also known as CD274) inhibits tumor-reactive T-cells via binding to the programmed death-1 (PD-1) receptor, rendering tumor cells resistant to CD8+ T cell-mediated lysis (1). Studies have shown that the inhibitory receptor PD-1 is expressed on tumor-infiltrating lymphocytes (TIL) while PD-L1 is expressed on tumor cells. Assessment of PD-L1 expression in combination with CD8+ TIL density may be a useful predictive metric in multiple cancers, including stage III NSCLC, hormone receptor negative breast cancer and sentinel lymph node melanoma (2-4). Clinical trials utilizing humanized chimeric antibodies that block inhibitory checkpoints, such as anti-PD-1 and anti-PD-L1, have demonstrated delayed tumor growth and increased survival (5). While identification of PD-L1 overexpression by IHC is not yet standardized, it has become increasingly important to identify these tumors, as a directed therapy may improve clinical outcomes in these patients (6). In cutaneous melanoma, the targeting of PD-1/PD-L1 has provided meaningful clinical benefit for patients in just the past 5-10 years (7). The use of IHC for protein identification, along with novel therapies, such as checkpoint inhibitors and vaccines, are generating new options for the treatment of cancer patients. The PD-L1 [CAL10] clone does not cross react with PD-L2.