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). This evidence concerns the gene AKT1 and cancer.