While ssDNA gap accumulation has been associated with chemosensitivity, arguing that it promotes cytotoxic DNA damage, this has been mostly investigated in specific genetic backgrounds (BRCA deficiency or PRIMPOL overexpression) upon treatment with 0.4 mM HU as a general condition of replication stress, or upon treatment with genotoxic chemotherapeutic agents such as cisplatin or PARP inhibitors13,15–19,22–26. The gene discussed is PRIMPOL; the disease is hyperinsulinemic hypoglycemia, familial, 4.