Interferon-γ signaling has been shown to regulate PD-L1 expression in cancer cells (Chen et al., 2012; Garcia-Diaz et al., 2017), and the combination of increased CD38 protein and mRNA signature (PD-L1, PD-L2, and CTLA4) associated with T cell exhaustion are representative of multiple mechanisms of immune evasion in this tumor type, with implications for immune checkpoint therapy (Chen et al., 2018; Sade-Feldman et al., 2018). Here, CTLA4 is linked to neoplasm.