As their experiments in HL1 cells showed that knockdown of the endogenous PKP2 of the cells in combination with co-expression of the p.(Arg635Gln) variant (as well as other BrS-related missense variants) with WT PKP2 led to a reduction in peak INa, they performed a rescue experiment in the iPSC-CM line derived from an ARVC patient with a homozygous c.2484C > T PKP2 frameshift loss-of-function variant [111] using lentiviral constructs containing WT-PKP2 and PKP2-R635Q. Here, PKP2 is linked to Arrhythmogenic right ventricular dysplasia.