In a uninephrectomized rat model characterized by sequential development of dysglycemia, renal dysfunction and renal cancer, we found activation of the RAS pathway, reduced expression of IGF-binding proteins and increased expression of HMGCR, protein kinase C ξ and Akt (or protein kinase B) which were reversed by treatment with RAS inhibitors, with reduced cancer growth, suggesting crosstalk between the RAS and HMGCR pathways [34]. The gene discussed is HMGCR; the disease is cancer.