It is well-established that tumors employ multiple strategies to evade T-cell surveillance, including (a) the downregulation of HLA class I and class II proteins (e.g., in melanoma, glioblastoma) [47,48]; (b) altered peptide processing via defects in proteasomes, TAP transporters, or cathepsins [49,50], (3) the secretion of immunosuppressive factors (e.g., TGF-β, PGE2, IDO) that inhibit T-cell function [51,52]. Here, CTSS is linked to melanoma.