Furthermore, Ikka-deficient lung ADCs contribute to a pro-tumor immunosuppressive milieu by upregulating TNF expression, which activates TNFR2/NF-κB/Foxp3 signaling to enhance the conversion of CD4 T cells to Foxp3 Treg cells in KrasD12GIkkaΔLU mice that have a wild-type immunological background before Ras activation and Ikka ablation in the lungs [41, 45]. This evidence concerns the gene CD4 and neoplasm.