We hypothesized that, because of the higher percentage of CD8+ T-cells in the B16F10-Fluc tumors of mice inoculated with B16F10-Fluc cells and KO MDSCs, tumor cells would be under pressure and would likely adapt resistance mechanisms to circumvent CD8+ T-cell-mediated killing, such as the expression of PD-L1 [40]. Here, CD8A is linked to neoplasm.