USP19 and cardiac hypertrophy: In order to confirm whether TAK1 and the downstream p38/JNK1/2 signalling contributes to the effect of USP19 on cardiac hypertrophy, iTAK1 was added to PE‐cultured cells to abolish the expression of phosphorylated TAK1 (Figure 6D), it was found that iTAK1 recovered the phosphorylated p38, JNK1/2 (Figure 6D), the cell size and hypertrophic markers (ANP and Myh7) (Figure 6B,C) to low levels in AdshRNA‐infected and even AdshUSP19‐infected NRCMs when compared to the iTAK1‐negative groups, and iTAK1 decreased these index to similar levels in AdshRNA and AdshUSP19 mice.