In the present study we show that: i) HIPK2 protein expression is lost in PTCs; ii) HIPK2 mRNA levels are up-regulated in follicular hyperplasia (FH) and reduced in PTC and in follicular variants of PTC (FVPTC); iii) loss of heterozygosity (LOH) affecting the HIPK2 gene locus can be detected in more than one third of PTCs; iv) RNA interference (RNAi) or overexpression of HIPK2 in PTC-derived K1 cells causes upregulation or downregulation respectively of Gal-3 expression. This evidence concerns the gene HIPK2 and familial hyperaldosteronism.