In cancer cells treated with decitabine or other epigenetic drugs inducing DNA demethylation and/or histone acetylation, the repressed production of T helper 1 (TH1)-type chemokines CXCL9 and CXCL10 by the tumor can be reversed, leading to increased infiltration of CD8+ T cells to tumor sites, arresting the tumor progression, and improving the outcome of adoptive T-cell immunotherapy in tumor-bearing mice [103]. Here, CXCL9 is linked to neoplasm.