For example, Tat-Beclin1–stimulated models showed increased Beclin1, LC3-II, and p62, mimicking our 1–2-week-old “enhanced initiation with p62 accumulation [37]“, whereas salvianin B in myocardial ischemia upregulated LC3/Atg5/Beclin1 and reduced p62, consistent with our 2–8-week-old normal autophagy [38]. The gene discussed is TAT; the disease is myocardial ischemia.