In the light of these considerations, the absence of a proficient p53 and the particular vulnerability of KRAS mutated tumors to dysregulated DNA damage repair mechanisms, do suggest that the combination of the Wee1 inhibitor with sorafenib might be useful new strategy for this sub-population of cancers but also for RET rearranged cells as reported by Levinson et al. 30. The gene discussed is TP53; the disease is cancer.