We found that CDK5 could directly phosphorylate ERK5 at Thr732, which suited the conservative sequence of CDK5(X-S/T-P-X).33 Further studies showed that knockdown of CDK5 decreased the phosphorylating level of ERK5 at Thr732, AP-1 and some of its target genes' expression, which was reversed when CDK5 was overexpressed without a ERK5 inhibitor in CRC cells. This evidence concerns the gene JUN and colorectal carcinoma.