Our experimental data showing that the drug-tolerant population of MDA-MB-231 is CD24+/CD44+ and has elevated levels of Jagged1 and Notch suggest that Notch-Jagged signalling also acts as an intercellular ‘phenotypic stability factor’ for the hybrid E/M phenotype; and is resonant with the emerging notion that carcinoma cancer stem cells (CSCs) lie mid-way on the ‘EMT axis’ [7,37,53–55], and that Notch-Jagged signalling is often implicated in maintaining CSC population and chemoresistance [15,35]. This evidence concerns the gene JAG1 and cancer.