Several mechanisms have been implicated in this insensitivity of ARID1A/EGFR‐comutated NSCLC to EGFR inhibitors, including the activation of compensatory signaling pathways (e.g., PI3K/Akt, JAK/STAT, and NF‐κB) and the promotion of epithelial to mesenchymal transition (EMT) and angiogenesis [47]. Here, ARID1A is linked to non-small cell lung carcinoma.