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One possible explanation for this impact is the decrease in Beclin-1 caused by the suppression of HIF1A, which could provide protection for cells

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Defining how these pathways evolve under sustained CD38 pressure and identifying when adenosinergic modulation becomes clinically relevant will be essential

*Correspondence: ngela Roco, Laboratory of Chemical Carcinogenesis and Pharmacogenetics, (CQF), Molecular and Clinical Pharmacology Program, ICBM - Insituto de Ciencias Biomdicas, Faculty of Medicine, University of Chile, PO Box 70111, Carlos Schachtebeck 299, Quinta Normal, Santiago, Chile e-mail: [email protected] This article was submitted to Pharmacogenetics and Pharmacogenomics, a section of the journal Frontiers in Genetics

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