Consistent with earlier analyses of the NCI-60 cell lines [19, 20] and with growing evidence for the role of epigenetic mechanisms in SLFN11 inactivation [21, 69, 81], we found that increased methylation of the SLFN11 promoter was negatively correlated with SLFN11 expression and increased resistance of SCLC lines to DNA-damaging agents (Supplementary Figure 3). The gene discussed is SLFN11; the disease is small cell lung carcinoma.