SLC30A6 (ZnT6) encodes a zinc transporter that lacks intrinsic transporter activity on its own but forms a functional zinc:proton antiporter heterodimer with SLC30A5, mediating zinc entry into organelles along the secretory pathway. As part of this zinc:proton antiporter complex, SLC30A6 contributes to zinc homeostasis within the early secretory pathway and regulates the activation and folding of enzymes such as alkaline phosphatases and those involved in phosphatidylinositol glycan anchor biosynthesis. SLC30A6 is relevant to multiple disease contexts. Structural variants affecting SLC30A6 have been identified in spastic paraplegia cases, with SPAST:SLC30A6 fusion transcripts documented in patients with final exon deletions, potentially explaining cosegregation of spastic paraplegia with dementia in some families 1. In cardiomyocytes, SLC30A6 overexpression induces mitochondrial dysfunction and epigenetic modifications associated with cellular dysfunction 2. At the population level, SLC30A6 shows relatively low genetic differentiation between populations (weighted-average FST = 0.015), suggesting weak natural selection pressures 3. Clinically, elevated SLC30A6 expression is associated with poor prognosis in pancreatic ductal adenocarcinoma, where higher expression correlates with unfavorable overall survival (HR = 1.90, p = 0.003) and involvement in oncogenic pathways including epithelial-mesenchymal transition and angiogenesis 4. In colorectal cancer, SLC30A6 upregulation may reflect increased early secretory pathway activity 5. Additionally, SLC30A6 has been identified as a druggable target associated with chr2 back pain variants in multi-ancestry studies 6.