Consistently, previous studies indicated that TKI treatment could potentially inhibit EGFR‐mediated Src activation and its downstream Akt‐dependent cell survival/proliferation pathways in EGFR‐mutated cancer cells to reduce their survival, while the expression and activity of Src has been linked with TKI sensitivity.[27] In contrast, we demonstrated that exposing cancer cells to CM from PCs did not affect ERK phosphorylation, a key component of the MAPK signaling pathway, regardless of TKI treatment, compared to cells exposed to CM from cancer cells (Figures S4F,G, Supporting Information). Here, EGFR is linked to cancer.