KLF5 and neoplasm: These results indicate that the increase in β-catenin and cyclin D1 levels in the intestine of mutant mice is primarily a consequence of ApcMin mutation, rather than KRASV12 over-expression and that the tumor suppressive effect of Klf5 haploinsufficiency in ApcMin/KRASV12 mice is due primarily to the ability of Klf5 to modulate ApcMin signaling.