In addition, 83 proteins were downregulated and 57 were upregulated only in FGFR4−/− CKD mice; enrichment analysis of these differentially expressed proteins suggests that deletion of FGFR4 upregulates pathways related to NADH activity, mitochondrial ribosomes, and mitochondrial translation and downregulates pathways linked to ATP transport, protein channel and fatty acid activity. This evidence concerns the gene FGFR4 and chronic kidney disease.