ABL1 and infection: In summary (Fig. 8), we report that P. aeruginosa T3SS triggers a rapid phosphorylation cascade involving CrkII/Abl → PKCδ → NLRC4, which leads to caspase-1 activation, culminating in the production of IL-1β and IL-18 pro-inflammatory cytokines, which in turn mobilize inflammatory leukocytes, such as neutrophils (PMNs) and macrophages (Møs), to the site of infection where they combat P. aeruginosa infection.