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<i>Drosophila</i>’s <i>white</i> gene encodes an ATP-binding cassette G-subfamily (ABCG) half-transporter. White is closely related to mammalian ABCG family members that function in cholesterol efflux. Mutants of <i>white</i> have several behavioral phenotypes that are independent of visual defects. This study characterizes a novel defect of <i>white</i> mutants in the acquisition of olfactory memory using the aversive olfactory conditioning paradigm. The <i>w¹¹¹⁸</i> mutants learned slower than wildtype controls, yet with additional training, they reached wildtype levels of performance. The <i>w¹¹¹⁸</i> learning phenotype is also found in the <i>w^apricot</i> and <i>w^coral</i> alleles, is dominant, and is rescued by genomic <i>white</i> and mini-<i>white</i> transgenes. Reducing dietary cholesterol strongly impaired olfactory learning for wildtype controls, while <i>w¹¹¹⁸</i> mutants were resistant to this deficit. The <i>w¹¹¹⁸</i> mutants displayed higher levels of cholesterol and cholesterol esters than wildtype under this low-cholesterol diet. Increasing levels of serotonin, dopamine, or both in the <i>white</i> mutants significantly improved <i>w¹¹¹⁸</i> learning. However, serotonin levels were not lower in the heads of the <i>w¹¹¹⁸</i> mutants than in wildtype controls. There were also no significant differences found in synapse numbers within the <i>w¹¹¹⁸</i> brain. We propose that the <i>w¹¹¹⁸</i> learning defect may be due to inefficient biogenic amine signaling brought about by altered cholesterol homeostasis.