While there are diverse strategies to inhibit hnRNP K-dependent pathways (e.g., p53-mediated transcription, Ras/Raf/MEK/ERK, c-Myc activation), post-translational modification associated with the subcellular localization of hnRNP K is very important for the development of novel therapy targeting hnRNP K. It is expected that in the near future, novel agents based on this concept will be applied as candidates to treat advanced RCC patients. This evidence concerns the gene MYC and renal cell carcinoma.