When examining subtype-specific transcriptional phenotypes in both KRAS mutant and wild type NSCLC, the proliferative tumor subtype were STK11/KEAP1 deficient in ~90% and ~75% of KRAS mutant and wild type tumors, respectively (85), and the proliferative tumor subtype appeared to respond to MEK inhibition (85). This evidence concerns the gene KRAS and neoplasm.