In turn, myeloid-derived IL-1β was found to selectively trigger non-canonical nuclear factor (NF)-κΒ activation in KRAS-mutant cancer cells via IL1R1 and inhibitor of NF-κΒ kinase α (ΙΚΚα), with the latter presenting a marked therapeutic target in mouse models of pre-metastatic and advanced lung cancer [16,30]. This evidence concerns the gene KRAS and cancer.