The disruption of SMAD4 in mouse tumors raises the possibility that B6 ApcMin/+ mice might share a similar genetic pathway of tumorigenesis as human CRC shown in Figure 1[12,13], especially considering that SMAD4 is distantly located from the ENU-induced ApcMin/+ locus (Figure 2). The gene discussed is SMAD4; the disease is colorectal carcinoma.