A potential therapeutic target to curb obesity and diabetes is thermogenic beige adipocytes. However, beige adipocytes quickly transition into white adipocytes upon removing stimuli. Here, we define the critical role ofcyclin dependent kinase inhibitor 2A (Cdkn2a)as a molecular pedal for the beige-to-white transition. Beige adipocytes lackingCdkn2aexhibit prolonged lifespan, and male mice confer long-term metabolic protection from diet-induced obesity, along with enhanced energy expenditure and improved glucose tolerance. Mechanistically,Cdkn2apromotes the expression and activity of beclin 1 (BECN1) by directly binding to its mRNA and its negative regulator BCL2 like 1 (BCL2L1), activating autophagy and accelerating the beige-to-white transition. Reactivating autophagy by pharmacological or genetic methods abolishes beige adipocyte maintenance induced byCdkn2aablation. Furthermore, hyperactive BECN1 alone accelerates the beige-to-white transition in mice and human. Notably, bothCdkn2aandBecn1exhibit striking positive correlations with adiposity. Hence, blockingCdkn2a-mediated BECN1 activity holds therapeutic potential to sustain beige adipocytes in treating obesity and related metabolic diseases.