The oncogenic potential of Rac1, mediated through ROS production, was highlighted in an earlier report where we showed that a constitutively active mutant of Rac1, namely V12, increased intracellular O2− production in human melanoma M14 cells leading to chemoresistance, while transient introduction of the dominant negative mutant N17 decreased O2− levels and enhanced apoptosis sensitivity. The gene discussed is RAC1; the disease is melanoma.