Systemic lupus erythematosus (SLE) is characterized by immune dysregulation and multi-organ inflammation that is frequently associated with the development of cardiovascular disease (1). Despite evidence from large observational studies linking the two diseases (2), a causal genetic relationship between SLE and CVD has never been established. Mendelian randomization (MR) is a causal inference method that measures and correlates the effect sizes of exposure-associated genetic variants in large-scale genetic association studies on traits of interest. We therefore read with great interest the recent report by Gao and colleagues (3) which used MR methods to explore the potential genetic link between lupus and a number of cardiovascular diseases.One of the primary findings in Gao et al. is the MR analysis showing that genetic susceptibility to SLE is associated with a higher risk of heart failure (HF). There is, however, some ambiguity concerning the datasets used for analysis. The main text states that the outcome GWAS for HF is derived from FinnGen and appears to be "All-Cause Heart Failure" (finn-b-I9_HEARTFAILURE_ALLCAUSE) which includes 23,397/194,811