While end resection was shown to be a source of DNA accumulating in the cytosol of genetically unstable tumor cells and even more so after additional experimental genome damage (44), we posit that steady state repair of double-strand breaks in genetically stable cells not exposed to genotoxic hazards does not occur on a large scale and therefore does not yield oligonucleotide waste in amounts sufficient to form cGAS ligands by random hybridization. The gene discussed is CGAS; the disease is neoplasm.