Other evidence suggests the alteration of the inflammatory response with abundant cytokine signaling pathways (interleukin 1, 2, 7, 10, and 15 signaling) in CF AEC post-RV infection could be explained by downregulation of RNF128 genes, which functions as an inhibitor of cytokine gene transcription and could interact with TBK1 (key hub of CF AEC response in our study here) kinase activity to enhance antiviral immunity. This evidence concerns the gene RNF128 and cystic fibrosis.