In vivo, the augmented NF-κB-dependent inflammatory reaction of Cyld−/− mice resulted in a lethal Escherichia coli pneumonia and more severe Haemophilus influenzae middle ear infection [26], [27], whereas increased activation of p38 protected Cyld−/− mice from lethal acute lung injury induced by Streptococcus pneumoniae infection [16]. Here, CYLD is linked to pneumococcal infection.