We suggest that in case of any deviations in gap filling function of polβ during BER, such as such polβ cancer-associated variants possessing aberrant BER function, the gap ligation by BER ligases can lead to the faulty repair events and formation of single deletion mutagenesis products, which in turn could lead to an interruption in the proper BER repair pathway coordination at the downstream steps. The gene discussed is POLB; the disease is cancer.