In these experiments, we noted that the tumor burden per mouse in cdkn1a−/− control animals (Figure 4D) was lower than in cdkn1a+/+ control animals (Figure 4B), most likely due to subtle differences in the overall genetic background of the animals used in the two experiments (see Materials and Methods) or possibly to a general lower tumor incidence in p21cip1 deficient animals [31],[32]. This evidence concerns the gene CDKN1A and neoplasm.