Such kind of anti‐cancer progression may be due to the expansion of previously untargeted (no tailored accurately) or undetected cell subclones.[6] In addition, the treatment that does not target estrogen receptor (ER) may result in incomplete suppression of cancer cells and lead to a phenotype switch from TNBC to ER‐positive enrichment.[6] In contrast, anti‐EGFR therapy may benefit when combined with anti‐ER treatment; it is suggested by the patient‐specific signaling signature (PaSSS) based predictions and was experimentally validated in two TNBC cell lines.[6]. The gene discussed is EGFR; the disease is cancer.