TRPA1 is a nonselective cation channel protein that has been implicated in the progression of fibrosis, but its role is cell type and context‐dependent.[18, 19, 30] In mice, pharmacological inhibition of TRPA1 ameliorated pressure overload‐induced cardiac hypertrophy and fibrosis,[19] suggesting a pro‐fibrotic role in TRPA1. This evidence concerns the gene TRPA1 and cardiac hypertrophy.