In addition, Ren et al. found that FUNDC1 and mitophagy were downregulated in a HFD-induced mouse model and that FUNDC1-knockout mice were more vulnerable to HFD-induced cardiac hypertrophy, fibrosis, and insufficiency, via interaction with FBXL2 in an inositol 1,4,5-trisphosphate receptor type 3 (IP3R3)-dependent manner (Ren et al., 2020). Here, ITPR3 is linked to cardiac hypertrophy.