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Simple Summary: In recent years, the incidence of cancer has been steadily increasing, necessitating a more urgent and in-depth understanding and exploration of this disease. During the process of literature review, we have discovered that the novel protein-coding gene, cartilage intermediate layer protein 2, has been partially associated with colorectal cancer in several studies. However, its role in other cancers remains elusive. Therefore, this study aims to explore the function and mechanism of cartilage intermediate layer protein 2 in pan-cancer. Our findings will enhance the understanding of the role of cartilage intermediate layer protein 2 in pan-cancer tumorigenesis and progression, especially in pancreatic cancer. This research could potentially establish cartilage intermediate layer protein 2 as a promising prognostic biomarker and immunotherapy target for cancers. The elucidation of its significance in pan-cancer will contribute to the development of more effective therapeutic strategies. Cartilage intermediate layer protein 2 (CILP2) facilitates interactions between matrix components in cartilage and has emerged as a potential prognostic biomarker for cancer. This study aimed to investigate the function and mechanisms of CILP2 in pan-cancer. We evaluated the pan-cancer expression, methylation, and mutation data of CILP2 for its clinical prognostic value. Additionally, we explored the immunological characteristics of CILP2 in pan-cancer and then focused specifically on pancreatic ductal adenocarcinoma (PAAD). The subtype analysis of PAAD identified subtype-specific expression and immunological characteristics. Finally, in vitro and in vivo experiments assessed the impact of CILP2 on pancreatic cancer progression. CILP2 exhibited high expression in most malignancies, with significant heterogeneity in epigenetic modifications across multiple cancer types. The abnormal methylation and copy number variations in CILP2 were correlated with poor prognoses. Upregulated CILP2 was associated with TGFB/TGFBR1 and more malignant subtypes. CILP2 exhibited a negative correlation with immune checkpoints in PAAD, suggesting potential for immunotherapy. CILP2 activated the AKT pathway, and it increased proliferation, invasion, migration, and epithelial–mesenchymal transition (EMT) in pancreatic cancer. We demonstrated that CILP2 significantly contributes to pancreatic cancer progression. It serves as a prognostic biomarker and a potential target for immunotherapy. [ABSTRACT FROM AUTHOR]