Consistent throughout literature, pathogenic FLI1 variants also repress transcriptional activity in validated FLI1 target genes including GP9, exhibiting predominantly cytoplasmic localization and in contrast, result in large, fused platelets that have electron-dense α-granules, characteristic of the Paris-Trousseau syndrome (78, 80, 81). This evidence concerns the gene FLI1 and Paris-Trousseau thrombocytopenia.