NPC1 (Niemann-Pick disease type C protein 1) is a lysosomal membrane protein that primarily functions as an intracellular cholesterol transporter, facilitating cholesterol efflux from lysosomes to maintain cellular cholesterol homeostasis 1. The protein operates through interaction with NPC2 to transfer cholesterol from late endosomes/lysosomes to cellular membranes 2. Beyond cholesterol transport, NPC1 regulates multiple cellular processes including mTORC1 signaling, where it normally promotes lysosomal degradation of STING to control innate immune responses 3. NPC1 also modulates autophagy and lysosomal proteolysis through its effects on mTORC1 activation 1. Loss of NPC1 function causes Niemann-Pick disease type C, characterized by lysosomal cholesterol accumulation, mTORC1 hyperactivation, and neurodegeneration 13. The protein's dysfunction has been implicated in other diseases including amyotrophic lateral sclerosis, where muscle cholesterol accumulation correlates with disease severity 2. Interestingly, NPC1 exhibits cholesterol-independent functions, such as stabilizing TGFBR1 in hepatocellular carcinoma by preventing its ubiquitylation and degradation 4. Additionally, NPC1 serves as an endosomal entry receptor for ebolaviruses, highlighting its role in microbial pathogenesis. Therapeutic targeting of NPC1-related pathways, particularly mTORC1 inhibition, shows promise for treating associated diseases 1.