RAB6C is a primate-specific retrogene encoding a small GTPase with altered functional properties compared to its parent RAB6A' 1. Unlike canonical Rab proteins that regulate intracellular membrane trafficking through GTP-binding-dependent effector recruitment, RAB6C has reduced GTP-binding affinity and instead localizes to the centrosome through its noncanonical GTP-binding domain 1. RAB6C plays a critical role in centrosome regulation and cell cycle progression; its overexpression induces G1 arrest while depletion generates tetraploid cells with supernumerary centrosomes 1. Clinically, RAB6C has emerged as a potential cancer biomarker. RAB6C promoter hypermethylation with corresponding reduced expression is associated with poor prognosis in squamous cell carcinoma of the tongue and cervical cancer, with diagnostic sensitivity and specificity of 70-100% [PMID:28255813; 2; 30]. Salivary DNA methylation of RAB6C shows comparable accuracy to tissue samples for cancer detection (AUC 0.984) 4. In bladder cancer, RAB6C overexpression promotes cell proliferation and invasion, which is antagonized by miR-218 5. Additionally, RAB6C-AS1 long noncoding RNA is overexpressed in multiple cancer types with tissue-dependent oncogenic or tumor-suppressive functions 6. RAB6C was also identified in genome-wide association studies as a locus associated with Raynaud's syndrome 7.