This latter observation suggests that 129X1B6 ApcMin/+ is more resistant to tumor development and that our F2 cross between BL6 and 129 mice may have actually resulted in underappreciation of the negative effects of NHE3 deficiency, and the observed colonic tumorigenicity would have been further enhanced if the cross were maintained on pure B6 background. Here, SLC9A3 is linked to neoplasm.