A recent study by Jungnickel et al. revealed that, in parallel with the infection-induced pulmonary neutrophilic inflammation, NTHi-dependent stimulation of both TLR2 and TLR4 in a transgenic mouse [(KrasLA1) with oncogenic Kras allele in the lung epithelium] additionally promotes the proliferation of Kras-induced early adenomatous lesion in the lung in an TLR-dependent manner (247). The gene discussed is KRAS; the disease is infection.