For example, myeloid-targeted deletion of KLF4 increased S. pneumoniae burdens, lung pathology, and barrier permeability, despite elevated systemic IL-10.46 Together with our findings of increased neutrophil-mediated killing, bacterial clearance, and barrier function in myeloid IL-10R–deficient mice, this suggests that total pathogen burden is a more informative indicator of pulmonary tissue damage during pneumococcal pneumonia than the presence of neutrophils alone. The gene discussed is KLF4; the disease is pneumococcal pneumonia.