Amongst these, we noted that shRNAs targeting CDK4, CDK6 or the CDK4,6 cyclin partner gene Cyclin D1 (CCND1) preferentially inhibited Rb-proficient TNBC TCLs (Fig. 2c), consistent with the hypothesis that inhibition of CDK4,6 activity restores cell cycle control in Rb-proficient TNBC tumour cells and elicits cell inhibition [32]. The gene discussed is RB1; the disease is neoplasm.