The chapter describes the use of double-stranded RNAs (dsRNAs) to target and silence the *glu-2* gene in *Caenorhabditis elegans* using microinjection or soaking methods. The poly(A) polymerase assay is also discussed, involving in vitro translation and gel analysis to assess RNA processing. The text then transitions to a detailed study on the role of the Forkhead transcription factor FOXO3a in protecting quiescent cells from oxidative stress. FOXO3a is shown to increase the expression of manganese superoxide dismutase (MnSOD) mRNA and protein, thereby enhancing cellular protection against reactive oxygen species (ROS). This mechanism is particularly important under conditions of glucose deprivation, where FOXO3a activation can prevent apoptosis and mitochondrial damage. The study also highlights the inverse relationship between FOXO3a and protein kinase B (PKB) signaling, which controls cell proliferation and protection from oxidative stress. The findings suggest that the PKB-Foxo module serves as a key switch in coupling cell cycle regulation, glucose metabolism, and protection from oxidative damage.The chapter describes the use of double-stranded RNAs (dsRNAs) to target and silence the *glu-2* gene in *Caenorhabditis elegans* using microinjection or soaking methods. The poly(A) polymerase assay is also discussed, involving in vitro translation and gel analysis to assess RNA processing. The text then transitions to a detailed study on the role of the Forkhead transcription factor FOXO3a in protecting quiescent cells from oxidative stress. FOXO3a is shown to increase the expression of manganese superoxide dismutase (MnSOD) mRNA and protein, thereby enhancing cellular protection against reactive oxygen species (ROS). This mechanism is particularly important under conditions of glucose deprivation, where FOXO3a activation can prevent apoptosis and mitochondrial damage. The study also highlights the inverse relationship between FOXO3a and protein kinase B (PKB) signaling, which controls cell proliferation and protection from oxidative stress. The findings suggest that the PKB-Foxo module serves as a key switch in coupling cell cycle regulation, glucose metabolism, and protection from oxidative damage.