In a study with decitabine on glioblastoma cells and patient samples, it was found that tumor cells showed increased expression of MHC I and tumor-associated antigens after decitabine treatment, and T cells presented an upregulated Fas ligand (CD95) in association with increased levels of INF-γ, TNF-α, IL-5, and CD107A (functional parameters of degranulation of cytotoxic T cells via the Fas pathway) of NY-ESO-1 specific T cells and concluded that the epigenetic agent sensitizes glioblastoma to the functionality of specific T cells [120]. The gene discussed is FAS; the disease is glioblastoma.