Previous reports point out that p62 is partially involved within cisplatin resistance in human ovarian cancer cells, possibly by modulating Keap1-NRF2-ARE signaling activities.46 Indeed, our results also revealed that suppression of p62 reduced the mammosphere-forming ability of the epirubicin-resistant MCF-7 cells (Figure 6D), a cell line that shows aggressive stem-like features and multidrug resistance.21 Collectively, our data strongly suggest p62 as a potential target to limit breast cancer stemness, thus overcoming BCSC-mediated drug resistance. Here, KEAP1 is linked to ovarian cancer.