CAMK2A and alpha thalassemia-X-linked intellectual disability syndrome: Recent studies of a mouse model of typical α-thalassemia X-linked mental retardation (ATRX) also demonstrated increased autophosphorylation of CaMKIIα at Thr286, decreased levels of spinophilin and PP1, and increased phosphorylation of two downstream CaMKII/PP1 substrates, Tiam1 and Kalirin-7 [67].