A constitutively activated FAK-Src signalling, as observed in our patients' megakaryocytes, leads to permanent actin polymerization and this may cause abnormal proplatelet formation, as shown by treatment of megakaryocytes with an inhibitor of actin assembly, cytochalasin [22], or by macrothrombocytopenia in mice genetically deficient of ADF or cofilin, two proteins involved in actin depolymerization [23]. This evidence concerns the gene PTK2 and Macrothrombocytopenia.