Thus, the enrichment of KIF5A, PEX5L, SLC13A1, SLC6A19, and TFAP2A in the aforementioned pathways indicates these ipr-DEGs are functioned through regulating the activity of transmembrane transport, biosynthesis, metabolism, and endosome and peroxisome systems to regulate the development of ccRCC and the dysregulation of these ipr-miRNAs regulated ipr-DEGs drives the generation of ccRCC samples with distinct clinical and biological characteristics (Supplementary Figure S12B). This evidence concerns the gene PRPS1 and nonpapillary renal cell carcinoma.