It has been demonstrated that decreased levels of iPLA2‐β disrupt the skeletal structure of the Golgi complex,3 trafficking from the Golgi complex to the endoplasmic reticulum,4, 5 and impair Vps26 and Vps35 levels, retromer functions and ceramides levels in Parkinson's Disease (PD) models, similar to α‐synuclein associated neurodegeneration.2 The gene discussed is VPS26A; the disease is Parkinson disease.