A soluble factor such as this could be a good candidate to signal from mutant PLCG2 BM cells to trigger G-CSF transcription from a non-hematopoietic cell, as required in this model of APLAID (Extended Data Fig. 8b); however, this is highly speculative. The gene discussed is CSF3; the disease is autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation.