The majority of identified pathways for example, cellular response to hypoxia, response to TGF-beta, serine/threonine kinase signaling pathway are well known to be de-regulated in ccRCC, although our analysis points to other, also interesting pathways that may contribute to ccRCC etiology, involving components of the homotypic fusion and protein sorting (HOPS)-tethering complex and mRNA poly(A) tail shortening (Table 1 and Table S3). The gene discussed is MARK2; the disease is nonpapillary renal cell carcinoma.