More specifically, this phenotype has been attributed to RCAN1, since transgenic mice overexpressing the human RCAN1-1 isoform present age-dependent hyperglycemia, impaired glucose tolerance, hypoinsulinemia, reduced β-cell secretion, reduced β-cell number, decreased insulin granule filling, and reduced mitochondria size in β-cell along with an aberrant mitochondrial reactive oxygen species production (Peiris et al., 2012). Here, INS is linked to Hyperglycemia.