Therefore, in APLAID, overproduction of G-CSF might act both locally by mediating trafficking of myeloid cells through the endothelium, as well as promoting local cellular survival within inflamed sites and systemically via increased proliferation of hematopoietic progenitor cells in the BM and spleen and the release of mature neutrophils into the blood. Here, CSF3 is linked to autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation.