Interestingly, Rac2 activation in neutrophils is primarily mediated by the dedicator of cytokinesis (DOCK) 2, an atypical guanine nucleotide exchange factor (GEF) that rapidly translocate to the plasma membrane in a phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependent manner upon stimulation, resulting in increased local CAcN polymerization (78, 79). DOCK2 is mainly expressed in peripheral blood leukocytes and DOCK2 deficiency causes an early-onset PID characterized by a T-cell defective chemotactic responses with bacterial and viral infections (no. 14 in Table 1 and Figure 1) (80). Here, DOCK2 is linked to pelvic inflammatory disease.