Therefore, in addition to the development of DSB-repair function by MYC in late-stage cancer cells, deregulated MYC, which leads to increased genomic instability, at least partly, via replication stress (see above), offers a chance for cancer cells to accumulate more genetic mutation and develop ways of evading the cytotoxic effects of anticancer drugs by, for example, downregulating tumour suppressor functions and/or upregulating drug efflux and detoxification (Figure 1). The gene discussed is MYC; the disease is neoplasm.