The study investigates the role of BMP signaling in regulating intestinal stem cell (ISC) self-renewal and its relationship with Wnt-β-catenin signaling. Using a conditional inactivation model of *Bmpr1a* in mice, the authors found that BMP signaling suppresses Wnt signaling, thereby controlling the balance of stem cell self-renewal. Specifically, PTEN, through the PI3K-Akt pathway, mediates the convergence of BMP and Wnt pathways in regulating β-catenin activity. In the absence of BMP signaling, PTEN levels are elevated, leading to increased β-catenin nuclear localization and enhanced ISC division. This results in an increase in the number of crypts and polyps, resembling human juvenile polyposis syndrome. The study also demonstrates that Noggin, an antagonist of BMP signaling, can abrogate BMP signaling and coordinate with Wnt signaling to fully activate β-catenin in ISCs. These findings highlight the importance of BMP signaling in maintaining intestinal homeostasis and preventing excessive stem cell proliferation.The study investigates the role of BMP signaling in regulating intestinal stem cell (ISC) self-renewal and its relationship with Wnt-β-catenin signaling. Using a conditional inactivation model of *Bmpr1a* in mice, the authors found that BMP signaling suppresses Wnt signaling, thereby controlling the balance of stem cell self-renewal. Specifically, PTEN, through the PI3K-Akt pathway, mediates the convergence of BMP and Wnt pathways in regulating β-catenin activity. In the absence of BMP signaling, PTEN levels are elevated, leading to increased β-catenin nuclear localization and enhanced ISC division. This results in an increase in the number of crypts and polyps, resembling human juvenile polyposis syndrome. The study also demonstrates that Noggin, an antagonist of BMP signaling, can abrogate BMP signaling and coordinate with Wnt signaling to fully activate β-catenin in ISCs. These findings highlight the importance of BMP signaling in maintaining intestinal homeostasis and preventing excessive stem cell proliferation.