An important contribution to the field came from Erb-Downward and colleagues,10 who assessed the lung microbiome in a small cohort of never-smokers, healthy smokers, and smokers with COPD. First, the authors found a similar number of bacterial 16S rRNA copies in BAL samples among all their subjects, arguing that rather than changes in the magnitude of the bacterial load, bacterial diversity might be a key differentiating factor. Indeed, in the two patients with the most severe COPD, there was evidence of reduced bacterial diversity as compared with the healthy or milder cases of COPD. This work clearly needs to be validated, but it does align with what might be expected, considering that lack of bacterial diversity in the intestinal tract is associated with an increased incidence of IBD.11,12 The key finding from Erb-Downward and colleagues10 was that the microbiota is different in distinct regions of the airways. Due to the small sample size, it is premature to draw strong conclusions; however, bearing in mind that diseases such as COPD can have localized foci of inflammation or tissue damage, one can speculate that a certain microbiota might associate with that site. Cause or effect still needs to be delineated. More recently, Sze and colleagues13 adopted a similar approach and assessed the microbiome in lung tissue of nonsmokers, healthy smokers, patients with severe COPD, and patients with cystic fibrosis (CF). Similar to Erb-Downward’s group, these authors showed that the bacterial load in the lung was comparable between healthy tissue and COPD lungs, but was significantly higher in CF lungs. Again, aligning with prior work, the authors showed that the constituents of the microbiota in healthy lungs and lungs with severe COPD were distinct.