Considering that NEFH has been suggested to be functionally associated with altered metabolism of tumor cells such as increased glycolysis via the AKT/β-catenin pathway 27, it can be hypothesized that NEFH alterations could contribute to the recently described metabolic shift of aggressive renal cancer cells found as a result of integrative genome-wide analyses of molecular alterations in ccRCC 9. The gene discussed is AKT1; the disease is neoplasm.