USP20 and cardiac hypertrophy: DUBs exert biological activities by degrading proteins or modulating function of substrates.[17] To delineate the candidate substrates of USP20 in cardiac hypertrophy, we utilized myocardial tissues from Ang II‐induced mice in vivo and mouse‐derived HL‐1 cells in vitro respectively to perform co‐immunoprecipitation (Co‐IP) coupled with liquid chromatography‐mass spectrometry/mass spectrometry (LC‐MS/MS) to screen potential USP20 substrates, the workflow for this interactome analysis is illustrated in Figure 4A.