(5) c-Jun. The role of c-Jun in regulating the CSC population was demonstrated by a recent study that c-Jun serves as an intermediary effector in c-Jun N-terminal kinase (JNK) signaling to promote stem cell phenotype in triple-negative breast cancer (TNBC) cells via the upregulation of Notch1 [65]. This evidence concerns the gene JUN and triple-negative breast carcinoma.