Interestingly, the proteomics detected the atypical GEF SmgGDS, a protein reported to interact with Rac1 that indirectly contributes to Rac1 regulation [42,46]; however, this atypical GEF was found to be dispensable for Rac1 hyperactivation in androgen-independent prostate cancer cells. This evidence concerns the gene ARHGEF2 and prostate carcinoma.