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We read with great interest a recently published article by Di Mauro et al. (2020) describing for the first time the use of a mimetic peptide (R7W-MP) to restore impaired forward trafficking and reduced half-life of L-type calcium channels (LTCC) caused by mutations in the CACNA1C gene, restoring channel function in vitro. The two novel mutations in the CACNA1C gene (Cavα1.2 T320M and Cavα1.2 Q428E) were found in patients with Brugada syndrome (BrS), one asymptomatic (T320M), and one with adoi:10.3389/fphys.2021.682567 pmid:34177625 pmcid:PMC8220137 fatcat:kogqlgbzbveu7fbqwnoxumpzwa