It becomes activated by the phosphatidylinositol 3-kinase-like serine/threonine kinases ATR (ataxia telangiectasia response) and ATM (ataxia telangiectasia mutated) through phosphorylation of Ser-317 and Ser-345 [28] followed by autophosphorylation of Ser-296 [30]. Here, MARK2 is linked to ataxia telangiectasia.