On the other hand, the EGFR pathway is known to mediate BCSCs.[59, 60] In clinical samples and patient‐derived xenografted models (PDXs), EGFR is highly correlated with stemness of breast cancer.[61, 62] Furthermore, EGFR inhibitors are reported to be responsible for elimination of BCSCs.[3] For downstream signaling, EGFR modulates BCSCs through both the PI3K‐AKT and MEK/ERK pathways in TNBC.[63, 64] Besides PI3K‐AKT signaling (Figure 4), our data indicated that ERK phosphorylation decreased upon SGCE knockdown (Figure S8B, Supporting Information), further supporting the above reports. This evidence concerns the gene AKT1 and breast carcinoma.