Based on these observations, it is plausible that overexpression of Bcl-2 in human cancers promotes the activation of the small GTPase Rac1 and its interaction with Bcl-2, resulting in an increase in intracellular O2•− that activates STAT3pTyr705 and its mitochondrial recruitment as well as the downstream transcription of target genes involved in proliferation and survival. The gene discussed is BCL2; the disease is cancer.