Thus, granule-mediated and TNFα/TNF-R1-dependent pathways are the main mechanisms underlying IFN-DC cytotoxic activity against most short-term glioblastoma cell lines obtained (Figure 2h), while FasL/Fas- and TRAIL/TRAIL-R2-dependent pathways are not critical, thus making a significantly smaller contribution to donor IFN-DC-mediated cytotoxic activity against glioblastoma cells. Here, FAS is linked to glioblastoma.