We also assess the role of ADAR1-mediated MAVS editing in mediating inflammation through the induction of IFN/NF-κΒ, and find that a lower level of ADAR1 or MAVS in B cell lymphoma does not correlate with an increase of IFN response as observed for solid tumors (such as lung adenocarcinoma or pancreatic cancer29). This evidence concerns the gene IFNA1 and lung adenocarcinoma.