While IL-17A expression is increased in many types of cancer and cancer-associated fibroblasts where it promotes chronic inflammation, tumor cell migration, invasion, and resistance to chemotherapy, and both IL-1 and IL-17A known to be a driver for NFκB-regulated genes and increases chemokines and cytokines in the tumor microenvironment [107], we do not see the direct effect of PARG on interleukin’s expression. The gene discussed is PARG; the disease is neoplasm.