Considering that in nerve cells, Cav1 and Cav2 subfamilies of VGCC [30,31] are thought to assemble as heteromeric complexes between the pore-forming α1 and the accessory subunits α2δ and β, modulating α1 gating and trafficking [32], it is presently unclear how patients [33] and mice [34] bearing a frameshift variant of Cacna2d4 coding for a truncated version (Tyr802*) of the accessory subunit of VGCC, α2δ-4, develop IRD with slow rod-cone degeneration (RCD4, OMIM # 610478, link accessed 17 October, 2022) while the complete loss of Cacna1f does not affect rod and cone viability in mice [25]. Here, CACNA2D4 is linked to Cone rod dystrophy.