Herein we provided the novel evidence showing that ATRA, a potent Pin1 inhibitor well known for its therapeutic effect on leukemia and other cancer [44, 79, 86], effectively increases endogenous CaV2.1 protein level in neurons, as well as notably reducing ER-associated degradation of EA2-causing CaV2.1 mutants. The gene discussed is CACNA1A; the disease is cancer.