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Objective: Prader‐Willi syndrome (PWS) is a multisystem genetic disorder. Unfortunately, none of several mouse models carrying PWS mutations emulates the entirety of the human PWS phenotype, including hyperphagia plus obesity. Methods: To determine whether housing at thermoneutrality (TN, 30 °C) permits the development of hyperphagia and obesity in the Snord116del PWS mouse model, the effects of housing three different ages of Snord116del and wild‐type (WT) littermates at TN versus room temperature (RT, 22–24 °C) for 8 weeks were compared. Results: Snord116del mice born and maintained at TN exhibited lower body weight curves, lower percentage fat mass, and lower food intake than WT mice at RT. In 4‐ to 6‐month‐old high‐fat diet–fed female mice, TN raised the Snord116del body weight curve closer to that of RT‐housed WT mice although the TN‐housed Snord116del mice did not gain more adiposity or exhibit greater food intake. In 6‐ to 8‐month‐old high‐fat diet–fed male mice, body weight, adiposity, and food intake of TN‐housed Snord116del mice remained far below levels in RT‐housed WT mice. TN elicited hypotonia in Snord116del adults and exacerbated mortality of Snord116del newborns. Conclusions: In none of three tested TN protocols were greater food intake, body weight, or adiposity induced in Snord116del mice compared with RT‐housed WT mice. [ABSTRACT FROM AUTHOR]