Ado can refer to multiple entities. It can stand for adenosine, a purinergic signaling molecule that modulates many physiological and pathological functions in the brain. Neuronal activity-induced extracellular Ado elevation is due to direct Ado release from somatodendritic compartments of neurons, depending on equilibrative nucleoside transporters [3].

It can also be an abbreviation for 2-Aminoethanethiol dioxygenase (ADO), a thiol dioxygenase that sulfinylates cysteamine and amino-terminal cysteines in polypeptides, playing a role in maintaining redox homeostasis in cancer cells through restraining polyamine levels and proline catabolism [1].

Moreover, ADO may refer to autosomal dominant osteopetrosis, characterized by generalized osteosclerosis, usually resulting from mutations in the chloride channel 7 (CLCN7) gene, with a wide disease phenotype [2].

Generation of the ADO knockout mouse (referring to 2-Aminoethanethiol dioxygenase) revealed high tolerance for ADO depletion in adult tissues. However, ADO depletion in cancer cells led to loss of proliferative capacity and survival, reducing xenograft growth. This indicates that ADO represents a vulnerability in cancer cells [1].

In summary, Ado in the form of adenosine has a role in neuronal signaling, while 2-Aminoethanethiol dioxygenase (ADO) is crucial for cancer cell redox homeostasis. The ADO knockout mouse model has been valuable in understanding the role of ADO in cancer, highlighting its potential as a target for cancer treatment. Autosomal dominant osteopetrosis (ADO) is a genetic disorder related to osteoclast function abnormalities, and understanding its genetic basis may aid in developing future therapies [1,2,3].