Upon IGF1 stimulation, pVHL-deficient RCC cells exhibit high rate of RACK1/IGF1R binding and up-regulate IGF1R tyrosine kinase activity, with subsequent phosphoinositide 3-kinase/serine-threonine kinase Akt (PI3K/Akt) signaling and matrix metalloproteinase-2 (MMP2) activity resulting in high RCC cells invasiveness (He et al. 2011). This evidence concerns the gene RACK1 and renal cell adenocarcinoma.