In summary, we have demonstrated that SDHD dysfunction does not change the absolute amount of PTEN expression, but instead is associated with increased oxidized PTEN, favoring the latter's nuclear location through activation of SRC, which weakens the PTEN anti-tumor function, thus resulting in apoptosis resistance and increased migration in both FTC and papillary thyroid carcinoma (PTC) cell lines. This evidence concerns the gene PTEN and differentiated thyroid carcinoma.