The chromatin immunoprecipitation (ChIP) assays showed that silencing of FBXW7 had a minor, if any, effect on the enrichment of RPB1, the largest subunit of RNAPII, at the transcription start site of c‐MYC or GAPDH, two commonly used genes for investigating RNAPII transcriptional regulation[18] (Figure S7B, Supporting Information), suggesting that FBXW7‐mediated RPAP2 degradation inhibits tumor growth independent of the transcriptional regulatory function of RPAP2 in modulating RPB1. Here, POLR2A is linked to neoplasm.