HPV-infected lung cancer cells upregulated IL-10 at the transcriptional level (involving phosphorylation of cAMP responsive element binding protein 1 and CCAAT/enhancer binding protein β) which stimulates an autocrine loop relying on the IL-10 receptor (IL-10R) by binding to IL-10R expressed by immune cells and IL-10 in turn may imbalance TH1 vs. TH2 tumor-specific immune responses cumulatively favoring tumor progression. This evidence concerns the gene IL10RA and lung cancer.