TP53 and neoplasm: We elected to investigate the genetic interaction of Nf2, Trp53, and KrasG12D further, by generating gRNAs to specifically target and disrupt the Nf2 and Trp53 loci (or a nontargeting control, gRNAscrm), which were then coinjected hydrodynamically with our KRASG12D expressing construct to define whether loss of these tumor suppressors can specifically cooperate with KRASG12D to promote tumor initiation.