6 appear to be the result of dysregulation of various cellular signaling events via the redox-sensitive Ras (for a deeper investigation see [7]). The misregulation of the redox signaling of Ras with its downstream cascades also has been linked to various disorders linked with immune and embryo developments. The Ras-dependent activation of Raf also leads to stimulation of a phosphorylation of Ets-like protein-1 and tumor necro- sis factor-α messenger RNA induction; both actions suggest that NO, through the Ras-dependent Raf-MEK1/2-ERK1/2 pathway, modulates a host’s defenses and the inﬂammation of T lymphocytes [92]. ROS-mediated signaling via Ras, NF- κB, and related transducers may link to embryopathies [93]. 5. Concluding Remarks Although, for many years, the generation of intracellular redox agents was viewed solely as the unregulated by-product of aerobic metabolism and other enzymatic processes, over the last years a growing number of reports have suggested that the production of intracellular ROS is tightly regulated and that these redox agents serve as intracellular signaling molecules being involved in a variety of cell signaling path- ways. Here we have reviewed studies reporting that mem- bers of the RasGTPase superfamily are able to regulate in- tracellular ROS production, and that the production of ROS by small GTPases is an important aspect of the function of these monomeric G-proteins. In addition, the functional cross-talk between some diﬀerent RasGTPase family members (see Rac1 and RhoA) appears strictly related to redox signaling. Finally, due to the presence of conserved redox-sensitive sequences, many of the Ras superfamily small GTPases have been shown to be targets of ROS regulation. Thus, redox agents, as upstream regulators and/or down- stream eﬀectors of redox-sensitive RasGTPases, strongly con- tribute to their overall biological function playing a key role in various cellular signaling events. Dysregulation of small GTPases by redox agents or dysregulation of redox signaling by small GTPases may signiﬁcantly alter cellular signaling pathways and lead to the pathological state. 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