In an attempt to evaluate if the modulation of S99 phosphorylation might be involved in the regulation of the events observed in Ankrd2 overexpressing OS-derived cell lines, and may, thus, be exploited to reduce cancer progression, all the biochemical and functional assays performed with wild-type Ankrd2 were contextually performed with the unphosphorylatable mutant form of Ankrd2, i.e., Ankrd2(S99A) (Figure 2 and data not shown). This evidence concerns the gene ANKRD2 and cancer.