Hu et al. (2022) found that ANGPTL8 can bind to LILRB3 and block downstream signalling pathways, such as those of AKT and glycogen synthase kinase-3β (GSK3β), thereby improving pathological cardiac hypertrophy. ANGPTL8 deficiency accelerates Ang II-induced cardiac hypertrophy and fibrosis (Su et al., 2021). Wang et al. (2022) also discovered a negative correlation between ANGPTL8 and left ventricular mass index (LVMI), indicating a protective effect of ANGPTL8 on cardiac remodelling. This evidence concerns the gene LILRB3 and cardiac hypertrophy.