Since the therapeutic targeting of ADAM17—with a highly specific and non-toxic prodomain inhibitor—in the preclinical KrasG12D LAC model displayed enhanced anti-tumour activity compared to anti-IL-6R antibodies [32,100], the use of ADAM17 inhibitors to specifically block pathological IL-6 trans-signaling in the lung promises to be a more effective and safer strategy to ameliorate disease states, including KRAS mutant LAC, driven by IL-6 trans-signaling. This evidence concerns the gene KRAS and neoplasm.