MAP1LC3B encodes a ubiquitin-like modifier protein essential for autophagosome formation and selective autophagy processes 1. The protein serves as a key marker of autophagy, with decreased MAP1LC3B puncta indicating impaired autophagy in disease states such as steatohepatitis 1. MAP1LC3B functions in multiple selective autophagy pathways, including mitophagy where it participates in the removal of damaged mitochondria through interaction with autophagy receptors like NDP52 and optineurin 2. The protein is recruited to autophagosomal membranes and works downstream of PINK1-mediated phospho-ubiquitin signaling in mitophagy 2. MAP1LC3B also mediates ER-phagy through interaction with the intrinsically disordered receptor TEX264, facilitating endoplasmic reticulum turnover during nutrient stress 3. Additionally, the protein is involved in STING-mediated noncanonical LC3B lipidation, which is critical for inflammasome activation and requires STING's proton channel activity 4. MAP1LC3B expression is regulated by transcription factor TFEB and can be induced by compounds like trehalose in neurodegenerative disease models 5. The protein's stabilization is also regulated through the VCP/p97-BECN1 pathway, where VCP/p97 UFMylation promotes BECN1 stability and facilitates autophagy initiation 6.