Homozygous loss of Mbd4 function also leads to accelerated intestinal tumor formation in mice that harbor an Apc allele that predisposes them to intestinal neoplasia (Millar et al., 2002), and mice with biallelic truncations of the Mbd4 coding sequence exhibit modestly increased mutation rates in colon cancer cell lines, including increased C>A mutation rates in certain lines (Bader et al., 2007). This evidence concerns the gene APC and colonic neoplasm.