When we compared transcriptomic data from RB1-defective TNBCs to those from TNBC with no apparent RB1 defect (Supplementary Data 3 and 4), we noted that RB1-defective TNBCs expressed significantly elevated levels of SKP2 and COPS1 (GPS1) mRNA (Fig. 4j, k, l, p < 0.05 for both TCGA [27] and Metabric [28] data, Wilcox rank sum test), suggesting that in these particular tumours, elevated SKP2 activity might buffer the effects of RB1 dysfunction. The gene discussed is SKP2; the disease is neoplasm.