The β-cell is equipped with at least six voltage-gated Ca²⁺ (Ca_V) channel α₁-subunits designated Ca_V1.2, Ca_V1.3, Ca_V2.1, Ca_V2.2, Ca_V2.3, and Ca_V3.1. These principal subunits, together with certain auxiliary subunits, assemble into different types of Ca_V channels conducting L-, P/Q-, N-, R-, and T-type Ca²⁺ currents, respectively. The β-cell shares customary mechanisms of Ca_V channel regulation with other excitable cells, such as protein phosphorylation, Ca²⁺-dependent inactivation, and G protein modulation. However, the β-cell displays some characteristic features to bring these mechanisms into play. In islet β-cells, Ca_V channels can be highly phosphorylated under basal conditions and thus marginally respond to further phosphorylation. In β-cell lines, Ca_V channels can be surrounded by tonically activated protein phosphatases dominating over protein kinases; thus their activity is dramatically enhanced by inhibition of protein phosphatases. During the last 10 years, we have revealed some novel mechanisms of β-cell Ca_V channel regulation under physiological and pathophysiological conditions, including the involvement of exocytotic proteins, inositol hexakisphosphate, and type 1 diabetic serum. This minireview highlights characteristic features of customary mechanisms of Ca_V channel regulation in β-cells and also reviews our studies on newly identified mechanisms of β-cell Ca_V channel regulation.