MALAT1 and diabetic kidney disease: In summary, we demonstrated that MALAT1 misregulation was involved in the progression of diabetic nephropathy, and we showed a potential feedback loop between MALAT1 and β‐catenin playing a role in high glucose‐associated podocyte impairment, with SRSF1 as a important participant potentially via changing the pattern of alternative splicing of gene targets through its physical binding to MALAT1; inhibition of MALAT1 broke the cascade and rectified podocytes dysfunction stimulated by high glucose (Fig. 8).