Functional redundancy is a key property of ecosystems and represents the fact that phylogenetically unrelated taxa can play similar functional roles within an ecosystem. The redundancy of potential functions (or DNA-level functional redundancy) of human microbiomes has been recently quantified using metagenomics data. Yet, the redundancy of functions that are actually expressed in the human microbiome has never been quantitatively explored. Here, we quantify the protein-level functional redundancy in the human gut microbiome for the first time using metaproteomics and network approaches. In particular, our ultra-deep metaproteomics approach revealed high protein-level functional redundancy in the human gut microbiome and high nestedness in the corresponding proteomic content networks (i.e., the bipartite graphs connecting taxa to their expressed functions). However, due to selective functional expression, the protein-level functional redundancy is lower than the DNA-level functional redundancy in the human gut microbiome. Using a consumer-resource population dynamics model, we found that such a selective functional expression contributes to the high richness and diversity in the assembled microbial communities. We further examined multiple metaproteomics datasets and showed that various environmental factors, including individuality, biogeography, xenobiotics, and disease, significantly affect the protein-level functional redundancy. In particular, inflammation and several xenobiotics significantly diminish the protein-level functional redundancy. Finally, by projecting the bipartite proteomic content networks into the unipartite functional similarity networks of genera, we discovered functional hub genera across individual microbiomes, suggesting that there may be a universal principle of functional organization in microbiome assembly.