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 reduced nicotinamide adenine dinucleotide activity, mitochondrial ribosomes, and mitochondrial translation and downregulates pathways linked to adenosine triphosphate transport, protein channel, and fatty acid activity (Figure 7d and e). Here, FGFR4 is linked to chronic kidney disease.