Furthermore, it has been reported that removal of terminal sialic acid moieties from complex glycan structures can normalize T-type currents in DRG neurons isolated from ob/ob mice, and reverse neuropathic pain in vivo [5], suggesting that glycosylation of Cav3.2 could possibly represent an underlying mechanisms contributing to the enhanced expression of the channel during diabetes. Here, CACNA1H is linked to diabetes mellitus.