Degradation of CDCA3 during G1 allows for wee1 accumulation during interphase, thereby providing a critical link between the anaphase promoting complex and SCF pathways in regulation of CDK1/cyclin B activity and thus mitotic entry and exit.[5] It was reported that everolimus resistance in prostate cancer cells was characterized by an increased level of cdk1 and cyclin B, driving the cells towards G2/M. Here, KITLG is linked to prostate cancer.