Analysis of pancreatic tissue from 26 human donors aged 20-80 revealed two fundamentally different types of senescent β-cells distinguished by their expression of cell cycle inhibitors CDKN1A and CDKN2A. CDKN1A-positive senescent cells lose their insulin-producing identity, show impaired glucose response, and release inflammatory signals that attract immune cells to pancreatic islets. Conversely, CDKN2A-positive senescent cells maintain their β-cell function and produce minimal inflammation. This discovery challenges the prevailing view that cellular senescence uniformly drives aging-related disease. Instead, it suggests some senescent cells may actually protect pancreatic function while others accelerate diabetes progression. The finding has profound implications for developing targeted therapies for age-related diabetes. Current senolytic drugs that eliminate all senescent cells indiscriminately could potentially remove protective CDKN2A-positive cells while leaving harmful CDKN1A-positive cells intact. Future diabetes interventions may need to selectively target only the maladaptive senescent cell population. This represents a paradigm shift toward precision senescence therapy, moving beyond the assumption that all senescent cells are inherently pathological.