HSP90 is known as the cancer chaperone which plays a crucial role in maintaining the stability of oncogenic drivers in lung adenocarcinoma.[23] Suppression of HSP90 leads to the degradation of oncogenic drivers and a loss of lung cancer cell viability.[23] Overexpression of HSP90 has been correlated with a poorer prognosis and chemoresistance in patients with non‐small‐cell lung carcinoma.[23, 24] The findings reported herein support ALA‐A2 inducing autophagy through downregulation of HSP90 expression in lung adenocarcinoma (Figure 5 and Table 2). This evidence concerns the gene HSP90AB1 and lung adenocarcinoma.