As expected, downregulation of SKP2, a downstream target of RB1, more efficiently suppressed the proliferation of RB1-deficient cancer cell lines in all 4 screens (Fig 2B) suggesting that RB1/SKP2 is a relatively robust SL interaction, being independent of the gene perturbation approach used (shRNA or CRISPR-Cas9) or the somewhat differing cell line panels used in different projects. The gene discussed is SKP2; the disease is cancer.