FIP1L1 and hematopoietic and lymphoid cell neoplasm: We speculated the presence of other genetic mechanisms of PDGFRA for IFP, such as chromosomal rearrangements (FIP1L1-PDGFRA and ETV6-PDGFRB) in hematopoietic neoplasms, PDGFRA amplification and gene rearrangement between PDGFRA and VEGFR2 in pediatric forms of glioblastoma, and somatic mutation in PDGFRB in fusiform aneurysms or Penttinen premature aging syndrome.[16]