TBC1D14 is a Rab GTPase-activating protein that serves as a negative regulator of autophagy by controlling membrane trafficking from recycling endosomes to autophagosomes 1. The protein localizes to Rab11-positive recycling endosomes and interacts with the autophagy kinase ULK1, where it regulates the early stages of autophagosome formation 1. Mechanistically, TBC1D14 functions through its interaction with the TRAPPIII complex, a multi-subunit tethering complex that acts as a GEF for RAB1, to maintain constitutive trafficking from peripheral recycling endosomes to the early Golgi apparatus 2. This trafficking pathway is essential for maintaining the cycling pool of ATG9 protein required for autophagy initiation 2. During amino acid starvation, TBC1D14 relocalizes from recycling endosomes to the Golgi complex, allowing transferrin receptor-positive membranes to contribute to forming autophagosomes 1. Beyond autophagy regulation, TBC1D14 has disease relevance in head and neck squamous cell carcinoma, where it suppresses lymph node metastasis by promoting DDX31 degradation and inhibiting ribosome biogenesis 3. Clinically, genetic variants in TBC1D14 have been associated with antibody response to oral cholera vaccine, suggesting broader immunological functions 4.