Based on the aggregate data available, Ambinder et al. support the hypothesis that "SIAIDs are the consequence of CMML.'' Several convincing mechanisms for the above hypothesis include abnormal monocyte behavior and signaling evident in clonal hematopoiesis causing overexpression of CD40 L leading to systemic lupus erythematosis (SLE), overexpression of ICAM-1 and sialic acid-binding Ig-like lectin 1 (Siglec-1), which facilitate the migration of monocytes to peripheral tissue, eventually leading to the increased expression of MHC-II and other costimulatory molecules. The gene discussed is ICAM1; the disease is chronic myelomonocytic leukemia.