EGFR and neoplasm: Despite its clinical success in selected populations, its efficacy in wild-type EGFR NSCLC and TNBC is limited, primarily due to innate and acquired resistance mechanisms, including secondary EGFR mutations (e.g., T790M), activation of bypass tracks (e.g., MET amplification), and the influence of the tumor microenvironment (TME) [18,19].