Our conclusion is supported by the following lines of evidence: (1) SKP2 is positively correlated with Aur-A in ccRCC tissues and cells, and protein and mRNA levels of SKP2 are elevated or reduced by Aur-A overexpression or silencing, respectively; (2) FOXO3A is a negative transcription factor for SKP2 [31, 32], and FOXO3A ubiquitylation and degradation by SKP2 mediating depends on the kinase activity of Aur-A; (3) the combination of Aur-A inhibitor MLN8237 and SKP2 inhibitor SZL P1-41 show a synergistic tumor growth inhibition in vivo and in vitro of ccRCC models. The gene discussed is SKP2; the disease is neoplasm.