Age-dependent accumulation of senescent cells in tissues and a progressive decline in cellular functions result in mislocalization of the nuclear and mitochondrial DNA in the cytoplasm. Sensing of self-DNA by the type I interferon (IFN)-inducible AIM2-like receptor (ALR) proteins in humans and mice results in production of type I IFNs (through activation of the cGAS-STING pathway) and activation of the AIM2 inflammasome, resulting in production of proinflammatory cytokines (IL-1 and IL-18). These cytokines alter the aging hallmarks. Dr. Choubey's laboratory has been interested in elucidation of the role of ALR proteins in altering the aging hallmarks and integration of their interactions. These studies are expected to improve the human health and lifespan.