While genetic resistance mutations often drive long term acquired drug resistance, the earliest events which enable residual cancer cells to regrow may be nongenetic.53 By exploring the consequences of sublethal apoptosis in persister cells, we uncovered a regulatory mechanism in which apoptotic DNase DFFB orchestrates transcriptional repression of ISGs, enabling escape from IFN-enforced growth arrest and facilitating initial persister cell regrowth (Figure 4j). The gene discussed is IFNA1; the disease is cancer.