Background: Cryptosporidium (C.) is a widespread opportunistic protozoan parasite that ranks with Giardia as the most common cause of diarrheal outbreaks globally. In addition to diarrheal manifestations, it was claimed to be a risk factor for GIT malignancy in immunocompromised animals. Objectives: studying the link between experimental C. parvum infection and ileocecal neoplasia. We investigated the effect of immune status, treatment and duration of infection on oncogenesis and its dependency on β-catenin/Wnt signaling pathway abnormalities. Methodology: C. parvum infected mice groups (immunocompetent and immune-suppressed; untreated and treated) were studied regarding oocyst shedding, dysplastic changes, cellular and genetic expression of β-catenin. Results: neoplastic changes were detected at higher rate and earlier time in C. parvum infected-immune-suppressed (ISP) mice with increased β-catenin expression at both cellular and genetic levels. Despite that, low grade dysplasia was detected in immunocompetent (ICP) mice as time progressed (i.e. 75 d.p.i.). No dysplasia was detected in nitazoxanide treated groups. Conclusion: our results demonstrate that, C. parvum infection is a risk factor for ileocecal dysplasia. The resulting pathology depends on the sintensity and duration of infection in addition to immune status of the host. Competent immune system is not an absolute protecting element against incidence of dysplasia but rather postpones it. β-catenin/Wnt signaling pathway is involved in C. parvum-induced intestinal dysplasia.