Background: Immune thrombocytopenia is an autoimmune condition marked by a reduced number of platelets in the blood, which can be caused by either a breakdown of platelets inside the blood vessels or the abnormal synthesis of platelets in the bone marrow. although autoantibodies have been shown as the principal factor in the pathogenesis of immune thrombocytopenia, also cellular immune modulation has been recognized to have a vital role in the pathophysiology of ITP. Aim of the Work: the pathogenesis of primary immune thrombocytopenia in pediatric patients. Patients and Methods: A Case-Control, analytical research that has been performed over one year after the approval of the research ethics committee on 70 participants (twenty-four) men & (forty-six) females with ages varying from (2 years) to (13 years) & an average age of (6.28±2.86) years old, Cases underwent history taking & clinical investigation. Laboratory investigations included CBC, DPC, ESR, bleeding time, C- C-reactive protein, and single nucleotide polymorphism. Conclusion: consanguinity was associated with ITP.  It is widely recognized that the pathogenesis of immune thrombocytopenia is significantly influenced by environmental & genetic factors. The susceptibility of cases to immune thrombocytopenia is influenced by single-nucleotide polymorphisms (SNP) of inflammatory cytokine loci, including IL-10, IL-17F, TNF-β, TNF-α, IL-6, TGF-β1, INF-γ, & IL0-1A. Additionally, various autoimmune disorders are related to genetic variants of inflammation-related genes, involving  CD226, CD24,IL-2, FCRL3,  ITGAM, IRF5,CARD8, NLRP3,  SH2B3, PTPN22, TNFAIP3, TRAF1, & STAT4.