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With aging, both the phenotype and function of NK cells are affected (Fig. 1). The number of existing subpopulations of NKs renders their evaluation difficult. Presently, we mostly uncovered the changes in the major subtypes characterized by the expression of CD56 and the basic activating and inhibitory molecules. The role of chronic, persistent viral infections is also difficult to separate from the aging process per se. A longitudinal study demonstrated that the late-differentiated CD56dim NK cells (CD57⁺ NKG2C⁺ FcRγ^–) may be driven less by chronological aging, even less by chronic disease severity, but far more by CMV infection [73]. Nevertheless, aging seems also to influence the accumulation of these dysfunctional NK cells. This has a profound functional implication for old subjects, such as increase in infections, malignancies, cardiovascular diseases, concomitant with the decrease in vaccine efficacy. They are also somehow ineffective in the senescent cell elimination. In the meantime, NK cells may be polyfunctional and cross-react with various microorganisms. The discrepancies in the results of studies in this field suggest that we need more longitudinal studies to be able to better asses the changes with aging and distinguish the effects of aging from latent chronic infections. The modulation of the phenotype and functions of these NK cells may be beneficial in increasing the health span of old subjects.