Hence, the reduced surface expression of CD44 in lung macrophages of COPD observed in our study (Figure2) has the potential to favour secondary necrosis of apoptotic cells (known to be increased in COPD[32,33]) and to prevent an adequate pro-resolution response (enhanced TGFβ, VEGF, and HGF macrophage release). This evidence concerns the gene CD44 and chronic obstructive pulmonary disease.