Combined with the recent data suggesting that 53BP1‐pathway defects in BRCA1 mutant, PARPi resistant tumour cells cause profound sensitivity to Polθi [17, 18] it also suggests that if Polθ inhibitors are to be used when PARPi or platinum resistance has occurred, this should be in those with 53BP1/Shieldin defects, and perhaps not in those where the dominant tumour clone has a BRCA1/2 reversion. Here, POLI is linked to neoplasm.