ATP10D is a P4-type ATPase that functions as a glucosylceramide (GlcCer) flippase, catalyzing ATP-dependent transport of GlcCer from the outer to inner leaflet of the plasma membrane 1. The protein contains conserved structural motifs in transmembrane domains, particularly a critical glutamine residue in TM4, that determine substrate specificity for GlcCer recognition 2. ATP10D localizes to the plasma membrane through N-terminal trafficking signals and plays a primary role in regulating plasma GlcCer homeostasis 34. Functionally, ATP10D expression reduces cellular hexosylceramide levels and facilitates GlcCer metabolism, with potential therapeutic relevance to Gaucher disease, a lysosomal storage disorder characterized by GlcCer accumulation 1. Genome-wide association studies identified ATP10D variants (rs2351791) associated with altered serum lipid profiles and cardiovascular disease risk, including coronary and intracranial atherosclerosis in elderly populations 52. Transgenic ATP10D expression in mice reduced high-fat diet-induced obesity by 25%, improved insulin sensitivity with 69% lower insulin levels, and decreased triacylglycerol levels, partly through reduced hepatic stearoyl-CoA desaturase 1 expression 6. However, ATP10D is not involved in Parkinson's disease pathogenesis despite associations with plasma GlcCer levels 4.