Notably, there was no significant change in the expression of Mal in the lungs of emphysematous Tlr4−/− mice (Figure 4E), and the lack of a role for Mal in the development of emphysema in human disease was also suggested by our observation that MAL gene expression was unaltered in human lung tissue from emphysema and control emphysema-free individuals (Figure 4F). Here, TLR4 is linked to pulmonary emphysema.