Previous studies have shown that NSCLC cells exhibit senescence‐like behaviors after knockdown of PTPN11 in a low‐serum medium, and inhibition of the XIAP gene increases senescent cell death by attenuating the binding of autophagic vesicles to lysosomes, thereby inhibiting the downstream process of autophagy.[55, 56] This is consistent with our finding that embelin and SHP099 induced elevated β‐galactosidase expression and a senescent phenotype. Here, PTPN11 is linked to non-small cell lung carcinoma.