A significant proportion of inv(3)/t(3;3) MDS and AML cases have activating mutations in RAS GTPase family member (NRAS or KRAS), or in other RAS-signaling pathway proteins, including PTPN11 (protein tyrosine phosphatase non-receptor type 11), and NF1 (neurofibromin 1), which promote dysregulated RAS signaling and uncontrolled proliferation52,77,79. This evidence concerns the gene NF1 and myelodysplastic syndrome.