To investigate the role of Dok-1, -2, and -3 in the development and malignant conversion of intestinal tumors, we crossed mice lacking Dok-1 and Dok-2, the closest homologs with redundant functions among Dok family adaptors (10), or Dok-3 knockout mice with ApcMin/+ mice (abbreviated as Apc mice), a mouse model of intestinal tumorigenesis bearing a heterozygous mutation in the tumor suppressor gene Apc (13, 14). This evidence concerns the gene DOK2 and intestinal neoplasm.