SPON2 and renal fibrosis: Interestingly, both genetic knockout mindin mice and HK‐2 cells with stably overexpressed mindin suppressed and promoted the levels of TGF‐β/Smad signalling pathway‐ and targeted‐related proteins, respectively, suggesting that mindin might exacerbate renal damage through activating the TGF‐β/Smad signalling pathway and the downstream targeted pro‐fibrotic proteins during renal fibrosis.