LITAF (lipopolysaccharide-induced TNF factor) is a dual-function protein involved in both endosomal trafficking and transcriptional regulation. In the cytoplasm, LITAF directs endocytosed growth factor receptors, including EGFR and ERBB3, to lysosomes for degradation, thereby attenuating downstream signaling. It recruits ESCRT complex components to membranes and interacts with the ubiquitin ligase NEDD4 to regulate protein degradation. In the nucleus, LITAF functions as a transcription factor that regulates inflammatory cytokine expression, including TNF-α, CCL2, CCL5, and IL-10, and may cooperate with STAT6 in this capacity 1. LITAF also serves as a surface receptor for pathogenic toxins; Bacillus cereus hemolysin BL binds LITAF on mammalian cells, triggering inflammasome activation and pyroptosis 2. Functionally, LITAF appears to suppress malignant phenotypes: in colorectal cancer, LITAF is downregulated and its re-expression inhibits stemness, migration, and metastasis through FOXO1-mediated SIRT1 regulation 3. Mutations in LITAF are associated with Charcot-Marie-Tooth disease type 1C, a demyelinating peripheral neuropathy, representing a rare genetic cause among CMT-linked genes 45. LITAF is also overexpressed in glioblastoma in a subset of patients and correlates with poor survival 6.