Previously, we demonstrated that CAV1 deficiency accelerates CGD,[3, 13] and other studies have shown that CAV1 deficiency promotes PKCζ‐mediated Sp1 activation.[36] Given that caveolae structures are composed of CAV1, PTRF, and SDPR, which mutually regulate each other's stability,[27, 29] we found that downregulation of SDPR mRNA by FXR‐miR30c/e pathway in miceC70‐KO led to a corresponding reduction in CAV1 and PTRF protein expression, resulting in caveolae instability. This evidence concerns the gene CAVIN2 and chronic granulomatous disease.