Background: Pathogenic variants in SCN5A, the gene encoding the cardiac Na{}^{+} channel \alpha-subunit Na{}_{\text{v}}1.5, result in life-threatening arrhythmias, e.g., Brugada syndrome, cardiac conduction defects and long QT syndrome. This variety of phenotypes is underlied by the fact that each Na{}_{\text{v}}1.5 mutation has unique consequences on the channel trafficking and gating capabilities. Recently, we established that sodium channel \alpha-subunits Na{}_{\text{v}}1.5, Na{}_{\text{v}}1.1 and Na{}_{\text{v}}1.2 could dimerize, thus, explaining the potency of some Na{}_{\text{v}}1.5 pathogenic variants to exert dominant-negative effect on WT channels, either by trafficking deficiency or coupled gating. Objective: The present study sought to examine whether Na{}_{\text{v}}1.5 channels can cooperate, or transcomplement each other, to rescue the Na{}^{+} current (I{}_{\text{Na}}). Such a mechanism could contribute to explain the genotype-phenotype discordance often observed in family members carrying Na{}^{+}-channel pathogenic variants. Methods: Patch-clamp and immunocytochemistry analysis were used to investigate biophysical properties and cellular localization in HEK293 cells and rat neonatal cardiomyocytes transfected respectively with WT and 3 mutant channels chosen for their particular trafficking and/or gating properties. Results: As previously reported, the mutant channels G1743R and R878C expressed alone in HEK293 cells both abolished I{}_{\text{Na}}, G1743R through a trafficking deficiency and R878C through a gating deficiency. Here, we showed that coexpression of both G1743R and R878C nonfunctioning channels resulted in a partial rescue of I{}_{\text{Na}}, demonstrating a cooperative trafficking of Na{}_{\text{v}}1.5 \alpha-subunits. Surprisingly, we also showed a cooperation mechanism whereby the R878C gating-deficient channel was able to rescue the slowed inactivation kinetics of the C-terminal truncated R1860X (\mathrm{\Delta }Cter) variant, suggesting coupled gating. Conclusions: Altogether, our results add to the evidence that Na{}_{\text{v}} channels are able to interact and regulate each other’s trafficking and gating, a feature that likely contributes to explain the genotype-phenotype discordance often observed between members of a kindred carrying a Na{}^{+}-channel pathogenic variant.