Previous studies demonstrated that mutations affecting components of the KCDCOMs were associated with the development of other tumors, including breast cancer, lung cancers and B cell lymphomas [20–23], The possible mechanism was considered that dysfunction of KCDCOMs could promote oncogene expression (e.g., BCL2) and decrease tumor suppressor gene expression (e.g., TP53 and SOCS3) [20, 22, 23]. This evidence concerns the gene TP53 and B-cell non-Hodgkin lymphoma.