Work by Ní Gabhann et al. (2014) reported a role for BTK in macrophage M1 polarisation, which was dependent on STAT1 and p65 phosphorylation, while O'Riordan et al. (2020) demonstrated that X‐linked immunodeficient (XID) mice subjected to polymicrobial sepsis had reduced M1 macrophages compared with wild‐type (WT) controls due to reduced NF‐κB and NLRP3 inflammasome activation. This evidence concerns the gene BTK and Sepsis.