A study in mice demonstrated that ethanol exposure suppresses the mir-29b-1 in developing cerebellar granule neurons, inducing apoptosis, while its overexpression protects against ethanol-induced neuronal death by regulating the SP1/RAX/PKR cascade [Qi et al. DOI:10.1074/Jbc.M113.535195]. In human cardiac stromal cells, the mir-29b-1 was significantly upregulated in arrhythmogenic cardiomyopathy patients, with its target genes enriched in extracellular matrix organization pathways [Rainer et al. DOI:10.1186/s12864-018-4876-6]. In human studies, the mir-29b-1 is upregulated in the anterior cingulate gyri of Parkinson's disease patients and downregulated in their blood, associating it with disease pathology [Das et al. DOI:10.1080/21655979.2021.2003667].