Upon APC11 knockdown using two distinct siRNA oligos, we observed that the neddylation levels of CUL5, but not CUL1, were upregulated in multiple cancer cell lines, including PLC/PRF/5, Hep3B, PANC‐1, and A549 cells (Figure3a; Figure S2a, Supporting Information), along with the accumulation of Cyclin B1 or securin, well‐known substrates of APC/C complex, serving as a positive control for APC11 knockdown (Figure 3a; Figure S2a, Supporting Information). The gene discussed is CUL1; the disease is cancer.