Efferocytosis by human and murine AMøs is significantly increased by in vitro treatment with clinically relevant doses of statins, macrolides, or corticosteroids.31,40,42,55,56 In mice, this effect of statins has also been demonstrated in vivo; it appears to be mediated by RhoA inhibition (thereby allowing activation of Rac-1, which is necessary for efferocytosis).56 Corticosteroids increase AMø efferocytosis by two processes: one rapid and dependent largely on SIRPα down-regulation; the other delayed yet sustained, dependent on new protein synthesis and associated with Mertk upregulation.31 The rapid corticosteroid action is nonadditive with statins, as anticipated, because both act on the Rac activation pathway. Whether chronic effects of statins and corticosteroids on efferocytosis are additive requires further study. By contrast, the effect of azithromycin on efferocytosis is additive with corticosteroids,31 implying that it results from an unrelated, currently undefined mechanism. The mucoregulatory drug carbocysteine also increases both efferocytosis by murine AMøs and clearance of apoptotic neutrophils from the lungs of mice.57 Collectively, these findings suggest that enhanced efferocytosis already occurs in many patients with chronic airways diseases, as one action of widely prescribed medications. However, no research has separated the direct antiinflammatory or antimicrobial effects of agents from their proefferocytic effect. Hence, the contribution of enhanced efferocytosis to improved clinical outcomes in inflammatory lung diseases is uncertain.