In addition, BNP levels were higher in patients with active SLE combined with HF.[75] In addition, long-term antimalarial (AM) therapy and elevated creatine phosphokinase could lead to an increased risk of BNP abnormalities, which may be able to predict AM-induced cardiomyopathy.[76] Our analysis suggested that the increased N-terminal pro-BNP was a risk factor for the development of SLE, further supporting these findings. The gene discussed is NPPB; the disease is hydrops fetalis.