Furthermore, our mechanistic elucidation revealed that the effects of circNAB1 on fibrosis were, at least partially, mediated through its interaction with transcription factors EGR1, Runx1 and Gadd45b, which are known key regulators of fibrotic processes and disease development.[34, 35, 36, 37] Our current study suggested that significantly elevated expression of circNAB1/NAB1‐356 in cardiac hypertrophy suppressed Runx1 and Gadd45b expression, through directly binding to their promoters and inhibiting fibrotic related transcription. Here, NAB1 is linked to cardiac hypertrophy.