However, dysregulated calcium handling in mutant rods, with depleted calcium stores and upregulated calcium and sodium influx via CSC distinct from VGCC, enlighten possible pathogenetic mechanisms linking faulty α2δ-4 to the mild cone-rod dystrophy reported in patients homozygous for the CACNA2D4 truncating mutation [33] and suggest cation-selective channels may be targeted to prevent a metabolic overload by reducing calcium and sodium entry. The gene discussed is CACNA2D4; the disease is cone-rod dystrophy.