Familial adenomatous polyposis (FAP) patients harbor mutations in the APC gene and will develop adenoma and early colorectal cancer. Taking biopsies from non-adenomatous (NA) and adenomatous (A) colonic mucosa of FAP patients, we investigated the early events associated with FAP using the intestinal organoid model. In addition to their high proliferative capacity, NA- and A-organoids were characterized by cysts and cysts with buds, respectively, suggesting abnormal maturation. A-organoids were enriched in the stem cell marker LGR5 and dependent on EGF and TGFβ for their growth. Downstream of EGFR, AKT, β-catenin and YAP were found to be activated in A-organoids. While the p110β isoform of PI3K was predominant in A-organoids and essential for their growth, p110α was associated with the immature state of NA-organoids. Accordingly, the present invention relates to a method of treating Familial Adenomatous Polyposis in a subject in need thereof comprising administering to the subject a therapeutically effective amount of a PI3K inhibitor.