The amelioration of inflammatory responses in the lung during pneumococcal pneumonia by ibrutinib may also result from inhibition of other Btk-dependent receptors that regulated S. pneumoniae-induced lung inflammation (Hommes et al., 2014; Branger et al., 2004; Albiger et al., 2007; van Lieshout et al., 2018), including TLR4, TLR9, TREM-1 and NLRP3 (Weber et al., 2017; Ito et al., 2015; Ormsby et al., 2011). Here, TREM1 is linked to pneumococcal pneumonia.