Our findings provide a PDCD11‐targeted therapeutic rationale for specially degrading the C‐MYC oncoprotein by efficiently harnessing the SCFSKP2‐possessed E3 ubiquitination activity, which results in a reduced SKP2 expression to avoid triggering SKP2‐promoted tumor progression (Figures 2, 3, and 5). This evidence concerns the gene PDCD11 and neoplasm.