Figure 4 illustrates how SIRT1-driven deacetylation allows tumor cells to evade senescence, withstand oxidative stress, and maintain proliferation under adverse conditions [63]. However, these effects are shaped by tumor-specific features, such as metabolic flexibility, mutational background, and tissue context, resulting in distinct biological consequences. The next section discusses how the redox-modulatory functions of SIRT1 contribute to cancer progression and therapy resistance in a cancer type-specific manner [62] (Figure 5). This evidence concerns the gene SIRT1 and cancer.