Our findings are therefore consistent with previous results showing that the luteinization process is associated with up-regulation of CDKN1B that accumulated during initial phases of luteinization and remained elevated until termination of the luteal function [59]. It was also demonstrated that inhibition of JAK3/STAT3 signaling significantly decreased viability of colon cancer cells due to apoptosis and cell-cycle arrest through down-regulation of cell cycle genes including cyclin D2 and up-regulation of CDKN1B [36]. Here, CCND2 is linked to colonic neoplasm.