Wang et al. (147) demonstrated that KuA (salidroside) mitigates neuronal cell death, ECM deposition, and inflammatory responses induced by LPS in NPCs through the activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, thereby contributing to the alleviation of IDD. Here, AKT1 is linked to intervertebral disk degenerative disorder.