Results gleaned from overexpression studies of human CP mutations in HCT116 cancer cells and expressing corresponding human CTC1 mutations into CTC1−/− MEFs strongly suggest that CP is due to failure to properly maintain the telomeric C‐strand, leading to telomere replication defects (Chen et al., 2013; Gu & Chang, 2013; Gu et al., 2012). This evidence concerns the gene CTC1 and cancer.