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In the past decades, several groups have found that drugs that harmine and other dual specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) inhibitors are able to induce proliferation of human -cell and increase islet mass in vitro and vivo, and its pro-proliferative effects primarily operate via translocation of nuclear factor of activated T-cells (NFAT) transcription factors to the nucleus, with the consequent transactivation of cyclins such as cyclin A, CDKs such as CDK1, and repression of CDK-inhibitors such as p15 INK4 , p21 CIP1 , and p57 KIP2 [42, 43]

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