SHH and Cowden disease: With possible relevance to human tumors, unlike previous models of Pten heterozygous mutant mice that model Cowden Syndrome or hamartoma syndromes33 or ones that involve embryonic conditional loss of Pten in all GCPs12, 13, we found that heterozygous loss of Pten in sporadic GCPs does not result in more aggressive tumors than activating SHH-siganling alone in rare GCPs.