Yet, a limited level of evidence exhibits that AAD, namely Type II diabetes mellitus (T2DM), can affect the biology of multipotent CPCs and promotes cellular senescence, per se, by upregulating pathologic SASP, including pro‐inflammatory cytokines (IL‐1α, IL‐1β, and IL‐6) and chemokines (MCP‐1 and MMP‐3), and suppress adult myocardial regeneration (Rota et al., 2006; Shakeri et al., 2018). This evidence concerns the gene IL1B and type 2 diabetes mellitus.