Objective To investigate the causal relationship between resistin and multiple myeloma (MM). Methods A two-sample Mendelian randomization analysis was conducted using genetic variants (SNPs) associated with resistin as instrumental variables and MM genome-wide association study (GWAS) data as the outcome event. Five analysis methods, including inverse-variance weighted (IVW), MR-Egger, weighted median, weighted model, and simple model were used to assess the causal impact of resistin on the risk of MM. Results None of the five analysis methods showed a causal relationship between resistin and multiple myeloma (P>0.05). Sensitivity analysis indicated consistent and robust results, with no evidence of horizontal pleiotropy, heterogeneity, outliers, or individual SNPs influencing the findings. Conclusion This Mendelian randomization study provides no support for a causal relationship between resistin and the risk of multiple myeloma.
