LITAF (lipopolysaccharide induced TNF factor) is a multifunctional protein that serves dual roles as both a transcription factor and an E3 ubiquitin ligase. As a transcription factor, LITAF regulates cytokine expression and inflammatory responses, with the ability to bind DNA and potentially synergize with STAT6 in transcriptional regulation 1. In its role as an E3 ubiquitin ligase, LITAF participates in protein degradation pathways, including the regulation of MCL-1 ubiquitination which affects mitochondrial autophagy 2. LITAF also functions in endosomal protein trafficking and targeting proteins for lysosomal degradation. The protein exhibits context-dependent effects in different diseases. In colorectal cancer, LITAF acts as a tumor suppressor, being downregulated in tumors and inhibiting cancer cell stemness, metastasis, and malignant behavior through regulation of the FOXO1-mediated SIRT1 signaling pathway 3. Conversely, in epilepsy, upregulated LITAF contributes to neuronal damage by promoting MCL-1 ubiquitination and inhibiting mitochondrial autophagy 2. LITAF is also associated with Charcot-Marie-Tooth disease type 1C, a demyelinating peripheral neuropathy 4. Additionally, LITAF serves as a cellular receptor for Bacillus cereus hemolysin BL toxin, contributing to host-pathogen interactions and inflammasome activation 5.