Therefore, we knocked down the expression of PlexinB1 on the basis of overexpression of SEMA4D, and the results showed that the role played by SEMA4D was greatly weakened, thus demonstrating that SEMA4D promotes the phosphorylation of PI3K/Akt in AML in a PlexinB1-dependent manner, thereby promoting the proliferation and survival of AML cells. The gene discussed is SEMA4D; the disease is acute myeloid leukemia.