This phenotype of resistance to aerodigestive tract carcinoma seen in Ip6k1 knockout mice is in direct contrast to the outcome of 4NQO treatment observed in Ip6k2 knockout mice (described earlier), which showed a higher incidence of carcinoma.91 These contrasting observations suggest that in aerodigestive tract epithelial cells, IP6K1 is responsible for promoting carcinogenesis, whereas the predominant function of IP6K2 is to prevent transformation by promoting apoptosis. Here, IP6K1 is linked to carcinoma.