In conclusion, our current study supports a differential requirement for Mal and MyD88 in TLR4-mediated emphysema, whereby Mal selectively promotes the pulmonary anti-apoptotic, but not oxidant suppressive, activities of TLR4, both of which appear to be essential for TLR4 signaling to preserve the normal architecture of the lung. Here, MYD88 is linked to pulmonary emphysema.