Binge eating (BE) is a heritable trait associated with eating disorders and involves episodes of rapid, large amounts of food consumption. We previously identified cytoplasmic FMR1-interacting protein 2 () as a genetic factor underlying compulsive-like BE in mice. is a homolog of which is one of four paternally-deleted genes in patients with Type I Prader-Willi Syndrome (PWS), a neurodevelopmental disorder whereby 70% of cases involve paternal 15q11-q13 deletion. PWS symptoms include hyperphagia, obesity (if untreated), cognitive deficits, and obsessive-compulsive behaviors. We tested whether haploinsufficiency (+/-) would enhance compulsive-like behavior and palatable food (PF) intake in a parental origin- and sex-dependent manner on two genetic backgrounds, including the BE-prone C57BL/6N () background and the BE-resistant C57BL/6J () background. mice showed increased compulsive-like behavior on both backgrounds and increased PF intake on the background. In contrast, maternal haploinsufficiency on the BE-resistant background induced a robust escalation in PF intake in wild-type males while having no effect in males. Notably, induction of behavioral phenotypes in wild-type males following maternal has previously been reported. In the hypothalamus, there was a paternally-enhanced reduction in CYFIP1 protein whereas in the nucleus accumbens, there was a maternally-enhanced reduction in CYFIP1 protein. Nochange in FMR1 protein (FMRP) was observed in mice, regardless of parental origin. To summarize, haploinsufficiency increased compulsive-like behavior and induced genetic background-dependent, sex-dependent, and parent-of-origin-dependent effects on PF consumption and CYFIP1 expression that could have relevance for neurodevelopmental and neuropsychiatric disorders.