Cases 1 and 3 exhibit varying degrees of hypoalbuminemia, which is a common outcome of disease activity and consumption in SLE patients and is the initiating factor for pleural effusion and peritoneal effusion, but such a large amount of pleural effusion, ascites, and elevated CA-125 cannot be fully explained by low protein, preferring a PPMS diagnosis. This evidence concerns the gene MUC16 and Pleural effusion.