Mutations within ion channels can cause functional alterations, including either loss or gain of function. Specific activation of the TRPA1 channel has been shown to be sufficient to trigger pain in humans [Heber et al, 2019]. The dbSNP database records five missense single nucleotide polymorphisms (SNPs) within the TRPA1 gene - R3C, R58T, E179K, K186N, and H1018R, with the second most frequent variant exceeding 10% in the general population. This study aimed to compare these genetic variants concerning their impact on established modes of activation in contrast to the most common form of TRPA1. By employing site-directed mutagenesis, the human TRPA1 channel variants were created and expressed in HEK293t cells for analysis using calcium microfluorimetry. Their responses to electrophilic (AITC and JT010) and non-electrophilic (Carvacrol and PF–4840154) agonists were examined. Since TRPA1 variants typically occur heterozygously, potentially leading to the formation of channels with mixed TRPA1 monomers, cotransfection experiments of the most frequent form with each of the SNPs were conducted using different agonist concentrations. Results indicated that each agonist triggered concentration-dependent activation of human TRPA1 channels, with the R58T variant consistently demonstrating a higher EC50 compared to other variants. The other identified SNPs did not significantly affect sensitivity to pharmacological agonists. Whether heterozygous subjects with the R58T mutation might manifest a decrease in TRPA1 responsiveness requires further investigation.