Moreover, some studies demonstrated that blocking NF-κB p65 and/or MAPK p38 and their specific inhibitors significantly attenuated the inflammatory response amplified by CD276 and reduced the production of pro-inflammatory cytokines and chemokines, and hence can be considered a potential therapeutic strategy to ameliorate the inflammatory damage caused by Streptococcus pneumoniae infections (19). This evidence concerns the gene CD276 and pneumococcal infection.