TINCR (Terminal differentiation-Induced Non-Coding RNA) encodes a highly conserved ubiquitin-like microprotein that functions as a tumor suppressor in epithelial cancers, particularly squamous cell carcinomas 1. The protein is upregulated by UV-induced DNA damage in a TP53-dependent manner and its decreased expression is prevalently found in skin and head and neck squamous cell tumors 1. TINCR suppresses tumor growth both in vitro and in vivo, with knockout mice showing accelerated tumor development following UVB carcinogenesis 1. However, TINCR exhibits context-dependent roles across different cancer types. In nasopharyngeal carcinoma, TINCR acts as an oncogene by binding ACLY protein, protecting it from ubiquitin degradation to maintain acetyl-CoA levels, which promotes lipid biosynthesis and activates the PADI1-MAPK-MMP2/9 pathway 2. Meta-analysis reveals that high TINCR expression correlates with larger tumor size and poor overall survival across multiple cancer types 3. Beyond cancer, TINCR functions in cardiac protection by acting as a competing endogenous RNA that sequesters miR-211-3p, thereby enhancing VEGFB expression and activating the VEGFB-SDF-1α-CXCR4 signaling pathway to alleviate cardiac hypertrophy 4.