Human aging is a very complex process that occurs in an intricate biological and physiological setting. Many changes occur with aging and among the most important are changes in immune reactivity associated with cell differentiation stages and the phenomenon of inflammaging, understood as subclinical inflammatory readiness, manifested by elevated levels of proinflammatory factors. It was stated for a long time that this tandem occurs in parallel or eventually sequentially. However, recent evidence points to the fact that, as both originate from chronic antigen stimulation, they mutually drive each other. In this context, inflammaging is considered the basis of most age-related diseases (ARD). In this review concerning human inflammaging, we argue that inflammatory diseases develop during whole life as a diverted (excessive) normal immune reaction to specific stressors. Thus, inflammaging may not be the cause of these diseases; however, it can be the trigger of clinical manifestation of ARD. In this context, the best intervention should aim to regulate the balance between pro- and anti-inflammatory signals and the more appropriate reaction to chronic stimulations to avoid/delay the appearance of associated diseases.