SCIN (scinderin) is a calcium-dependent actin filament-severing protein that plays crucial roles in cytoskeletal regulation and cellular processes. As an actin-severing protein, SCIN disrupts F-actin cytoskeleton organization when accumulated, as demonstrated in Sertoli cells where its buildup caused cytoskeletal disorder and disassembly 1. The protein exhibits complex roles in cancer biology, with context-dependent effects. In prostate cancer, SCIN knockdown inhibited cell proliferation and induced G0/G1 cell cycle arrest through regulation of cell cycle genes including p21Waf1/Cip1 and cyclin A2 2. Conversely, SCIN expression increases during gastric cancer progression from normal mucosa through chr7 atrophic gastritis to gastric cancer, correlating with poor survival and serving as an independent prognostic factor 3. In nasopharyngeal carcinoma, SCIN promotes cancer progression through the NF-κB signaling pathway, with depletion leading to decreased proliferation, invasion, and migration while increasing apoptosis 4. SCIN also modulates the tumor immune microenvironment and correlates with immune checkpoint markers 3. Additionally, SCIN has been identified as a disease-associated microglia marker gene in neurodegeneration models 5. The protein's regulation involves autophagy-lysosome degradation pathways and acetylation modifications 1.