 Cells lacking the ability to transport or phosphorylate dATP have been shown to exhibit increased resistance to the toxic effects of excessive dATP, suggesting that the toxicity of dATP is dependent on the ability to intracellularly phosphorylate dATP.As such, some treatments for ADA focus on reducing dATP phosphorylation by the targeted inhibition of the responsible deoxynucleoside kinases, such as adenosine kinase and deoxycytidine kinase.Deoxycytidine administered intravenously has also been used as an ADA treatment, although a clinical study found that deoxycytidine had only limited clinical effects on the T-cell immunity of ADA patients without discounting that some patients may respond more significantly to deoxycytidine therapy.