To determine the impact of β3 acquisition on the spontaneous development and progression of pancreatic cancer, we crossed mice from the previously developed24 triple mutant model of tamoxifen-inducible PDAC (i-KPC; KrasLSL-G12D/Tp53flox/flox/Pdx1-CreER), with mice expressing a conditional homozygous loss of Itgb3 (i-KPC-β3KO; KrasLSL−G12D/Tp53flox/flox/Itgb3flox/flox/Pdx1-CreER) (Figure 4B). Here, PDX1 is linked to pancreatic neoplasm.