To gain a more detailed understanding of the effects already described and thereby provide a basis for clinical benefit, we have investigated and characterized this relationship between ATR and POLA1. First, we applied a well-described cellular model of ATR-deficiency in the human colorectal cancer cell line DLD-1 [16,21,22,46], consisting of parental DLD-1 cells (subsequently referred to as ATR+/+ cells) and a derived DLD-1 cell clone homozygously harboring the a hypomorphic ATR Seckel mutation (subsequently referred to as ATRs/s cells). The gene discussed is POLA1; the disease is colorectal cancer.