Epidemiological studies have identified obesity as a risk factor for numerous chronic diseases such as adult onset diabetes, hypertension, and hypercholesterolemia. In both humans and laboratory animals, high-fat diets have been shown to cause obesity. Increases in dietary fat lead to increased energy consumption and, consequently, significant increases in body fat content. CD36 has been implicated in fat perception, preference, and increased consumption, but it is yet to be tested using a behavior paradigm. To study the effect of CD36 on fat taste transmission and fat consumption, four CD36 knockout (experimental) mice and four Black 6 wildtype (control) mice underwent 20 days of fat preference and perception testing. Both groups of mice were exposed to foods with progressively increasing fat content (10%, 12.5%, 15% 17.5%, 20%, 45%) in order to assess the effect of CD36 on fat preference. Afterward, the mice were subjected to an aversive conditioning protocol designed to test the effect of CD36 on fat taste perception; development of a conditioned taste aversion was indicative of ability to taste fat. Especially, knockout mice exhibited diminished preference for and reduced consumption of fat during preference testing and were unable to identify fat taste as the conditioned stimulus during aversive conditioning. A repeated measures ANOVA with Bonferroni correction revealed a significant main effect of group on fat consumption, energy intake, and weight. Linear regression revealed CD36 status to account for a majority of observed variance in fat consumption across both phases of the experiment. These results implicate CD36 in fat taste perception and preference and add to the growing body of evidence suggesting fat as a primary taste.