What these changes might be remains to be determined, however we note that in tumour cells with both BRCA1 and 53BP1 defects (where Polθi synthetic lethality is relatively profound), for the full degree of Polθi resistance to emerge, the dysfunction in BRCA1 and 53BP1 may have to be compensated for (as opposed to just a compensatory change in BRCA1 or 53BP1). This evidence concerns the gene POLI and neoplasm.