Our findings that illustrate the importance of FAK mediated Tyr357 activation of YAP are consistent with the recent studies that highlight EGFR‐FAK‐YAP/TAZ regulation as a mechanism of cancer resistance through nullifying the Hippo kinases.[32, 38] Considering that long‐term treatments with osimertinib lead to the development of resistance amongst NSCLC patients through YAP‐mediated oncogenic bypass as one major pathway,[39] the identification of agrin as mechanosensor for EGFR as well as YAP/TAZ target gene in sustaining tumor mechanotranduction is of significance. This evidence concerns the gene EGFR and non-small cell lung carcinoma.