Although these studies begin to dissect the mechanisms by which FAM13A could contribute to COPD pathogenesis, many of them are limited by a reliance on murine models which, because of a 5′ rearrangement in the Fam13a gene, express only the short isoform of Fam13a (www.ensembl.org/Mus_musculus/Transcript/Summary?db=core;g=ENSMUSG00000037709;r=6:58909075-59001534;t=ENSMUST00000089860) (19), limiting the relevance of these results for human FAM13A function. The gene discussed is FAM13A; the disease is chronic obstructive pulmonary disease.