Cisplatin was shown toyield only marginal tumor control, whilepaclitaxel–carboplatin was ineffective relative to untreatedcontrols. This well-documented chemoresistancereflects the distinctive KP tumor biology, establishing a high yetappropriate bar for proof-of-concept evaluations aligned with clinicalneed and translational development in this very aggressive lung tumormodel, in which both KRAS and TRP53 are altered. This evidence concerns the gene TP53 and neoplasm.