Combined with our experimental results, we conjectured that Emi1 reduced UBCH10 consumption by inhibiting ubiquitin chain extension between UBCH10 and CyclinB1, and inhibited the ubiquitination degradation of CyclinB1 protein, resulting in high expression of Emi1, UBCH10 and CyclinB1 in tumor tissues. The gene discussed is UBE2C; the disease is neoplasm.