Aging is an evolutionary paradox. Several hypotheses have been proposed to explain it, but none fully explains all the biochemical and ecologic data accumulated over decades of research. We suggest that senescence is a primitive immune strategy which acts to protect an individual’s kin from chronic infections. Older organisms are exposed to pathogens for a longer period of time and have a higher likelihood of acquiring infectious diseases. Accordingly, the parasitic load in aged individuals is higher than in younger ones. Given that the probability of pathogen transmission is higher within the kin, the inclusive fitness cost of infection might exceed the benefit of living longer. In this case, programmed lifespan termination might be an evolutionarily stable strategy. Here, we discuss the classical evolutionary hypotheses of aging and compare them with the pathogen control hypothesis, discuss the consistency of these hypotheses with existing empirical data, and present a revised conceptual framework to understand the evolution of aging. Electronic supplementary material The online version contains supplementary material available at 10.1134/S0006297922120021.