Key limitations include: (1) estimation of on‐target effects of drug use only (these models do not estimate potential off‐target effects); (2) lack of precision to robustly identify modest but potentially meaningful effects for some targets, including HMGCR inhibition; and (3) the possibility of survival bias, given that dyslipidaemias increase mortality prior to late‐onset PD, which might bias findings toward spurious inverse associations with PD risk. This evidence concerns the gene HMGCR and Parkinson disease.