Therefore, our data together with previous reports from other groups suggest that it is likely that the differences in the sensitivity of individual cell lines against CHEK1 inhibition could be explained by a loss of G1 control in general, rather than by p53 status alone; thus, CHEK1 inhibition by miltefosine can efficiently target both P53 mutant and WT CRC cells. This evidence concerns the gene CHEK1 and colorectal carcinoma.