TP53 and neoplasm: Next, we hypothesized that U14 would interfere with p53-mediated tumor suppression and cooperate with the KrasG12D oncogene to drive tumor formation.77 To test U14’s biological impact in vivo, we engineered lentiviral vectors that contain the FLP recombinase and a double-floxed inverted orientation (DIO) cassette of U14 or eGFP (LV-Flp-DIO-U14 or LV-Flp-DIO-eGFP), which we delivered through intranasal inhalations into the lungs of Frt-Stop-Frt (FSF)-KrasG12D; Rosa26-CreERT2 mice78,79, where a premature stop codon prevents KrasG12D expression in the absence of recombination.