Recent findings demonstrated that STK11/LKB1 alterations are associated with lack of response to PD-1 inhibitors efficacy, regardless of KRAS mutations or PD-L1 expression status,26,28 suggesting that different combinations of P53, STK11 and EGFR mutations were associated with different tumour microenvironments and may predict clinical response to PD-1 blockade.28 Unfortunately, neither P53 nor LKB1 status were known for KRAS-positive NSCLC patients included in our study because of the lack of tumour tissue available for molecular analysis. This evidence concerns the gene STK11 and neoplasm.