Besides cases in which HIF1α display very low expression due to 14q deletion, in many ccRCC, HIFs are constitutively stabilized through genetic inactivation of the von Hippel-Lindau (VHL) gene or mutations in TCEB1 (Elongin C), which impairs the function of the multimeric complex (VHL, Elongin B and C, Rbx1, Cul2) responsible for HIF ubiquitination [7, 8]. This evidence concerns the gene ELOC and nonpapillary renal cell carcinoma.