To assess the impact of immune aging on tumorigenesis in this model, we initiated tumors in young and aged K;H11LSL-Cas9 mice using a barcoded Lenti-sgRNA/Cre pool containing vectors targeting key nodes of the antitumor immune response, including antigen presentation (B2m and Tap2), IFNGR1 signaling (Ifngr1, Jak1, Stat1 and Irf1) and immune tolerance (Cd274 and Cd47) and performed Tuba-seq after tumor development (Extended Data Fig. 3a,b). Here, TAP2 is linked to neoplasm.