Building on such work, a recent study conducted by Wang et al. demonstrated the potential of miR-216a to act as a therapeutic target in T1D through its negative regulation of phosphatase and tensin homolog (PTEN) expression levels; the administration of a miR-216a mimic in a murine model of T1D increased beta cell proliferation, decreased PTEN expression, and improved insulin secretion in vivo [62]. The gene discussed is INS; the disease is type 1 diabetes mellitus.