The frameshift variant NM_000212.3(ITGB3):c.325del (p.Val109SerfsTer?) is predicted to cause a premature stop codon in biologically-relevant-exon 4/15 and is predicted to lead to nonsense mediated decay in a gene in which loss-of-function is an established mechanism (PVS1). The variant is absent from gnomADv4.0.0 (PM2_supporting). The variant has been found in at least one individual with GT, ClinVar entry (SCV000891200.1) by the Molecular Diagnostics Laboratory, M Health Fairview: University of Minnesota. The patient is compound heterozygous with variant of uncertain significance NM_000212.3(ITGB3):c.778-2A>G, phasing not confirmed. The patient had bleeding since childhood, abnormal aggregation, and flow cytometry low levels of GPIIb/IIIa. Patient information is consistent with GT but insufficient for PP4. In summary, this variant meets the criteria to be classified as Likely Pathogenic for autosomal recessive Glanzmann Thrombasthenia based on the ACMG/AMP criteria applied, as specified by the ClinGen PD VCEP: PVS1 and PM2_supporting (VCEP specifications version 2.1.0).