Moreover, it demonstrates that ALS-T2DM-IgGs immunocapture CaVα2δ1 subunits and thereby enhance CaV1 channel-mediated Ca2+ influx, resulting in altered [Ca2+]i dynamics and, consequently, impaired mitochondrial function, insulin secretion, and cell viability. The gene discussed is CAV1; the disease is amyotrophic lateral sclerosis.