Specifically, KrasG12D Trp53R172H (LSL‐KrasG12D/+; LSL‐Trp53R172H/+) mice[23, 24] were crossed with Ptf1a‐CreERT2 mice[25, 26] to generate KPP (LSL‐KrasG12D/+; LSL‐Trp53R172H/+; Ptf1a‐CreERT2) mice, which harbor mutant Kras and Trp53 to induce spontaneous pancreatic tumor formation. Here, PTF1A is linked to pancreatic neoplasm.