Gaifullina AS, Lazniewska J, Gerasimova EV, et al. - In order to report the causal association between homocysteine and the development of mechanical allodynia, researchers here used a rodent model of experimental homocysteinemia. Pharmacological inhibition of T-type calcium channels led to reversal of homocysteinemia-induced mechanical allodynia. Further, the in vitro studies show that homocysteine intensifies recombinant T-type calcium currents via raising the recycling of v3.2">Ca_v3.2 channels back to the plasma membrane through a protein kinase C–dependent signaling pathway that needs the direct phosphorylation of v3.2">Ca_v3.2 at specific loci. The findings, altogether, indicate the presence of an unrecognized signaling pathway that changes the expression of T-type calcium channels, and may potentially contribute to the development of peripheral neuropathy associated with homocysteinemia.