GABARAPL1 is a ubiquitin-like modifier protein that functions as a critical regulator of autophagy and cellular homeostasis. As part of the LC3/GABARAP protein family, GABARAPL1 plays essential roles in autophagosome maturation, specifically during later stages of autophagosome development rather than phagophore elongation 1. The protein serves as an autophagy receptor, facilitating selective degradation processes including mitophagy and Golgiphagy through interactions with LC3-interacting region (LIR) motifs 2. GABARAPL1 undergoes alternative lipidation to phosphatidylserine during non-canonical autophagy, providing a molecular signature distinct from conventional ATG8-PE conjugation 3. In disease contexts, GABARAPL1 dysfunction contributes to pathological processes: its downregulation during cerebral reperfusion exacerbates ischemic stroke injury by impairing astrocytic glycophagy 4, while it serves as a ferroptosis-related diagnostic marker in rheumatoid arthritis 5. The protein also functions in selective protein aggregate clearance, coordinating with HYPK to degrade polyneddylated proteins during proteotoxic stress 6. Unlike other GABARAP family members, GABARAPL1 displays complex tissue-specific regulation and is highly expressed in the central nervous system 7.