To understand the functional consequences of microbial community changes in IBD, we first functionally profiled gene families in all metagenomes using HUMAnN2, and then summed their abundances according to Enzyme Commission (EC) number annotations (see Methods and Supplementary Dataset 6). We applied the above-described linear modeling approach to this enzyme abundance data, revealing 568 enzymes that were differentially abundant (DA; FDR-corrected q50% of enzyme copies in >50% of samples,” then E. coli alone dominated 220 DA enzymes, owing in part to that species' strong enrichment in IBD and exceptionally thorough functional annotations. While some enzymes in this category may indeed have mechanistic connections to IBD, others may simply expand (or shrink) in copy number alongside their source genomes (whose abundance is changing for reasons unrelated to encoding of that particular enzyme)