However, multiple growth factor pathways, such as MAPK/JNK, PI3K/AKT, and VEGF signaling show comparatively greater enrichment in ASXL1 mutant disease than in overtly fibrotic MPN, suggesting that the lack of ASXL1 specifically enhances receptor tyrosine kinase signaling in MPN (Fig 4). This evidence concerns the gene MAPK8 and myeloproliferative disorder.