Claspin’s role as a checkpoint adapter protein, in which inactive Chk1 localises to Claspin to facilitate Chk1’s activation by ATR, is dependent upon the phosphorylation of Claspin’s Chk1 binding domain (CKBD); it has been shown that whereas casein kinase 1 can perform this phosphorylation in normal cells, DDK can perform this Claspin phosphorylation in cancer cells, thereby facilitating Chk1 activation [90,91] In combination, these results highlight the key role of DDK in mediating the response to replication stress. This evidence concerns the gene CLSPN and cancer.