It is unlikely that Bcl-2 and STAT3 compete for the same binding site on Rac1; however, it is plausible that in cancers with Bcl-2 overexpression, the induced GTP loading onto Rac1 promotes its interaction with STAT3 as well as phosphorylation of STAT3 as a result of redox changes or induced conformational change. Here, RAC1 is linked to cancer.