Salmeterol was cytotoxic at 10<sup>-4</sup> M and inactive at 10<sup>-8</sup>-10<sup>-6</sup> M. These findings indicate that the established anti-inflammatory benefits of ICS/LABA in COPD do not extend to augmentation of efferocytosis in this acute, serum-free in vitro setting and that pharmacological restoration of efferocytosis in COPD-a defect implicated in the pathogenesis and progression of comorbid lung cancer-will likely require strategies targeting the efferocytic machinery itself (e.g., MerTK, Rac-1, MFG-E8) rather than relying on current inhaled therapy. The gene discussed is MERTK; the disease is chronic obstructive pulmonary disease.