However, we did not observe a consistent pattern of chromosomal/gene alterations in the majority of samples/tumors between KRASG12D single transgenic mice and KRASG12D TAK1/CASP8ΔAc RIPK3-/- mice (Fig. 3i, j), arguing against the hypothesis that TAK1 deficiency mediated late stages of tumor promotion through changes in chromosomal stability. Here, RIPK3 is linked to neoplasm.