In accordance with a role for TLR signaling in host defense against pneumococcal pneumonia, MyD88 deficient (Myd88-/-) mice were reported to show a profoundly enhanced growth of pneumococci and a strongly reduced survival after intranasal infection with serotype 4 or 19F S. pneumoniae strains [18]. This evidence concerns the gene MYD88 and pneumococcal pneumonia.