In our previous study, we demonstrated that, in poorly differentiated thyroid carcinomas (PDTCs) and ATCs, the occurrence of a gain-of-function p53 mutation not only leads to the loss of the capability to downregulate Gal-3 but it acquires a de novo ability to stimulate its expression and induce chemoresistance [19]. This evidence concerns the gene TP53 and thyroid gland carcinoma.