We hypothesize that SASP, through its known inhibition of NF-κB and other immunomodulatory pathways, may indirectly suppress GM-CSF signaling or production within the alveolar microenvironment. Clinical data observations indirectly supporting this association include several reported cases of SASP-induced agranulocytosis that recovered rapidly with GM-CSF administration [11]. The gene discussed is NFKB1; the disease is Absence of circulating granulocytes.