EGFR and neoplasm: In cases where first‐ and second‐generation EGFR‐TKIs fail to inhibit the binding of ATP to the EGFR tyrosine kinase active site, and where third‐generation EGFR‐TKIs inadequately inhibit T790M‐mutation EGFR, silibinin could effectively suppress tumor initiation and development by blocking downstream signaling pathways in tumor cells [75].