As it was mentioned before, TP53/KRAS mt NSCLC tumors are related to an inflammatory microenvironment, enriched in TILs, have an increased presence of neoantigens and high PDL1 expression levels, whereas LKB1 inactivation in KRAS mt NSCLC tumors generally generates a suppressive immune microenvironment which could be linked to the lack of response to antiPD-1/PD-L1 blockade alone described in some studies (27–29). This evidence concerns the gene KRAS and non-small cell lung carcinoma.