In conclusion, mitoJNK localization disrupted the normal physiological functions of the mitochondria during ALI/ARDS, and selective inhibition of JNK and mitochondrial SH3BP5 (also known as Sab) binding with Tat-SabKIM1 can block deterioration from ALI/ARDS. The gene discussed is SH3BP5; the disease is acute respiratory distress syndrome.