This dichotomy highlights the heterogeneous nature of pSS and the multifactorial etiology of secondary ITP within this disease spectrum.[29] The lack of significant predictive value for a positive Schirmer test and other serological markers (Anti-SSA, Anti-SSB, Rheumatoid Factor, Anti-Ro52 Antibodies) suggests that secondary ITP development may not be directly mediated by these factors or that their roles may be overshadowed by more potent disease drivers. This evidence concerns the gene TRIM21 and autoimmune thrombocytopenic purpura.