KRAS and neoplasm: By using genetically modified mice permitting the oncogenic overexpression of mutant Kras in bronchial club epithelial cells expressing Clara cell secretory protein (CC10), Ji et al. showed an overwhelming neutrophil attraction to the TME accompanying LUAD formation and identified mutant Kras tumor-elaborated CXC chemokines (and their human orthologues IL-8 and CXCL-5) as the crucial mediators for this mechanism [49].