Biological mechanisms that render patients with NSCLC recalcitrant to ICB include alterations or functional mutations resulting in the inactivation of the tumor suppressor gene STK11/LKB1 and a consequent reduction in tumor-infiltrating lymphocytes22–25, inactivating mutations of KEAP1 (refs. 26,27), low expression of PD-L1, and alterations in antigen-presentation pathways. This evidence concerns the gene STK11 and neoplasm.