Inthe present study, we evaluated the role of 131I in cell proliferation,apoptosis and cell cycle arrest in a thyroid cancer cell line, together with theexploration of the possible underlying mechanism (increased expression ofBTG2 gene-mediated activation of the JNK/NF-κB pathways).131I significantly inhibited cell proliferation as assessed in terms ofcell-viability, enhanced cell apoptosis by down-regulating Bcl2 gene,and promoted cell cycle arrest at G0/G1 phase by down-regulatingCDK2 gene. This evidence concerns the gene BCL2 and thyroid gland carcinoma.