Mechanistically, HIV infection increases HIPK2 protein stability by promoting oxidative stress which inhibits the seven in absentia homolog 1 (SIAH-1)-mediated HIPK2 proteasomal degradation [69].Thus, the inhibition of reactive oxygen species (ROS) by N-acetylcysteine (NAC) abrogates the HIV-induced HIPK2 upregulation and reduces fibrosis, confirming the positive role of HIPK2 in kidney fibrosis [67]. Here, HIPK2 is linked to HIV infectious disease.