AKT1 and neoplasm: The main mechanism of EGFR‐TKI is to selectively bind ATP binding sites in the tyrosine kinase domain of EGFR in cells, block the phosphorization and activation of tyrosine itself in EGFR molecules through the Akt‐MAPK pathway, and inhibit RAS/RAF/MAPK, PI3K‐Akt, and other downstream signaling pathways and lead to apoptosis of tumor cells.13