RASEF (Rab45) is a large, atypical Rab GTPase containing an N-terminal EF-hand calcium-binding domain, coiled-coil motif, and C-terminal Rab homology domain 1. It functions as a Rab GTPase that acts as a dynein adapter protein, activating dynein-mediated transport on microtubules in a calcium-independent manner 2. RASEF exhibits self-interaction through its coiled-coil region and localizes to the perinuclear area in a guanine nucleotide-dependent manner 1. It regulates zymogen granule formation and secretion in pancreatic acinar cells and participates in vesicle-mediated transport. RASEF has divergent roles in cancer depending on tissue context. In colorectal cancer, high RASEF expression correlates with significantly better prognosis and associates with mismatch repair gene expression, suggesting a tumor-suppressor function 3. Conversely, in lung cancer, elevated RASEF promotes cell growth through enhanced ERK1/2 signaling and associates with poor prognosis 4. In uveal melanoma, RASEF promoter methylation silences the gene, with homozygosity and methylation associated with decreased survival, supporting a tumor-suppressor role 5. Additionally, RASEF hypermethylation mediates cigarette smoke-induced pulmonary artery remodeling in hypertension models, and RASEF overexpression reverses these pathological changes 6.