Since the inactivation of STK11 by mutational or non-mutational mechanisms is associated with an inert tumor immune microenvironment and lower PD-L1 expression [155,156], it has been suggested that co-occuring KRAS and STK11 (KRAS/STK11) alterations were associated with poorer response to ICIs for patients with NSCLC. This evidence concerns the gene STK11 and neoplasm.