Furthermore, cellular redox state is coupled to actin cytoskeleton dynamics [37]: for example, changes in redox signaling downstream different small GTPases can downregulate RhoA activity and stress fiber formation through Rac1 because tumor cells are almost invariably subjected to different sources of oxidative stress, such as altered metabolism and mitochondrial function or hypoxia, which has a profound impact on different aspects of tumor progression; therefore, a better understanding of this regulatory layer is warranted. This evidence concerns the gene RHOA and neoplasm.