Some of the reviewed pathways initiated by hyperglycemia coincide with mechanistic targets of successful pharmaceutical interventions, such as TxNIP assembly that was seen to be mechanistically inhibited by verapamil through the calcium influx blockade (see Fig. 4 and section Calcium-induced inhibition of TxNIP assembly in β-cells), and ER stress directly targeted by imatinib through inhibition of cytosolic ABL kinase transport (see Fig. 4 and section Imatinib-induced mediation of β-cell ER stress). This evidence concerns the gene TXNIP and Hyperglycemia.