However, alongside the known dysfunction of cyclin D genes, recent GEP studies have demonstrated that a high proportion of protein biosynthesis genes, specifically ribosomal protein genes representing end-points in MYC, NF-κB, and MAPK signalling pathways, are also concurrently overexpressed in hyperdiploid tumours [54, 55]. This evidence concerns the gene NFKB1 and neoplasm.