PDE10A encodes a phosphodiesterase that regulates intracellular signaling by hydrolyzing both cAMP and cGMP, with higher affinity and catalytic efficiency for cAMP. The enzyme plays a critical role in controlling cyclic nucleotide levels in the striatum, a brain region essential for movement and cognition control. Pathogenic variants in PDE10A cause autosomal dominant striatal neurodegeneration, with affected individuals presenting chorea as a predominant hyperkinetic movement disorder 1. Recent evidence suggests that PDE10A inhibition may have therapeutic potential in cancer therapy; in preclinical models, PDE10A inhibition suppressed ovarian tumor growth while simultaneously protecting against doxorubicin-induced cardiotoxicity through antagonism of cGMP/PKG and cAMP/PKA signaling pathways 2. Approved drugs targeting PDE10A include pentoxifylline, dipyridamole, and ibudilast, which are already established as safe drug targets. Genome-wide studies have identified variants in PDE10A under natural selection in the Bajau people of Southeast Asia, correlating with increased spleen size and enhanced oxygen storage capacity for breath-hold diving, indicating the gene's broader physiological relevance to hypoxia tolerance 3.