An elegant functional genetic study demonstrated that Cdh1, a core member of AJs, acts as an invasion suppressor in vivo; targeting a transgene encoding a dominant-negative Cdh1 molecule to the oncogene-expressing pancreatic β cells markedly accelerated tumor progression and led to significantly increased frequencies of invasive carcinomas and to the development of lymph node metastasis in this same mouse model of PNET [8]. This evidence concerns the gene CDH1 and primitive neuroectodermal tumor.