SCRIB (scribble planar cell polarity protein) is a scaffold protein that functions as a key regulator of cell polarity and tissue organization. It forms part of the lateral polarity complex along with DLG and LGL proteins, which is crucial for establishing apical-basal polarity in epithelial cells and maintaining apical junctions 1. SCRIB serves as a tumor suppressor, with its loss promoting cancer development through multiple mechanisms. In pancreatic ductal adenocarcinoma, SCRIB deficiency cooperates with oncogenic mutations to enhance invasive cancer development and metastatic dissemination by reducing IL1α levels, impairing cancer-associated fibroblast activation, and increasing YAP activation for enhanced cell survival 2. SCRIB also regulates the Hippo pathway through its interaction with TAZ, where disruption of SCRIB-TAZ complexes leads to TAZ nuclear accumulation and promotes cancer stem cell properties in breast cancer 34. Additionally, SCRIB functions in immune regulation, being required for adequate CD86 expression and IL-12 production in human dendritic cells, ultimately affecting T cell activation 5. Clinically, SCRIB expression is decreased in human pancreatic cancer, and its mislocalization is associated with poorer patient outcomes, establishing SCRIB as both a tumor suppressor and potential biomarker 2.