KRAS- and MYC-driven mouse lung adenocarcinomas had a marked increase in chemokine (C–C motif) ligand 9 (CCL9) and interleukin-23 (IL-23) inflammatory signalling molecules in the stroma resulting from MYC activation.126 These molecules facilitate a tumour-promoting microenvironment by supporting angiogenesis, recruiting macrophages and eliminating tumour-suppressive T, B and NK cells. The gene discussed is KRAS; the disease is neoplasm.