In the realm of aging theories, hyperfunction theories have emerged, suggesting that aging results from the inappropriate activation of developmental programs in adulthood. This perspective doesn’t necessarily contradict the idea of aging as a consequence of unrepaired damage. Instead, it views hyperfunction as either part of the damage or the primary cause of aging. Research guided by hyperfunction theory aims to identify harmful genes and suppress their activity. This approach highlights the importance of theory in driving research strategies to develop more effective therapies for aging. As evolutionary theories of aging evolve, new approaches are needed to study genetic contributions to age-related decline. Recent adaptations of evolutionary aging theories shed light on the role of continued gene activation in aging processes. The decline in natural selection pressure after sexual maturation leads to the expression of genes that were once beneficial for growth but become harmful in later life. Targeting hyperactive or hypoactive genes during aging could offer promising therapeutic interventions. While traditional frameworks attribute aging to the accumulation of molecular damage, recent research challenges this notion. Hallmarks of aging may not directly cause physiological decline but rather serve as symptomatic markers of deterioration. Understanding the role of these hallmarks in aging remains a complex puzzle. By identifying and studying late-acting hyperfunctional genes, researchers can delve into optimizing gene expression levels in aging individuals. A combination of omics techniques and healthspan screenings could provide valuable insights into the mechanisms of physiological aging. Ultimately, a shift towards practical research based on hyperfunction theory could lead to significant advancements in the field of aging.