Inflammaging, the chronic low-grade inflammation that accompanies aging, is recently implicated in the pathogenesis of diabetes-related disorders.4,5 During aging, cell senescence proceeds through an early senescent-response phase followed by the senescence-associated secretory phenotype (SASP) response.5,6 It is recognized that a heavier burden of senescent cells (SCs) together with SASP in diabetes leads to tissue disruption.7,8 The activity of Interleukin (IL)−1β represents the early SASP response,9 one of the specific determinants of aging.10,11. Here, IL1B is linked to diabetes mellitus.