In hematological malignancies, C-terminally truncated ASXL1 mutant protein significantly weakens the transcriptional regulation of BAP1-ASXL1-FOXK1 / K2 complex, downregulates the expression of multiple tumor suppressor genes, and then regulates glucose metabolism, hypoxia perception, JAK-STAT, and other tumor-related signaling pathways, promoting proliferation and self-renewal of leukemia cells [43]. This evidence concerns the gene SOAT1 and hematologic disorder.