Therefore, we hypothesized that chimeric proteins may have 2 related pathogenic mechanisms in AML: Firstly, the original promoter shape was changed, and normal ERG gene expression was not down-regulated, leading to dysregulation of the regulatory network, which regulate 3 major signaling pathways to impact the differentiation and proliferation of myeloid cells (Fig. 6); Secondly, it disrupts the regular metabolism of RNA splicing regulation. The gene discussed is ERG; the disease is acute myeloid leukemia.