In this work, we confirmed a significant increase in the expression levels of AMPK, PGC-1α, and SIRT3 in miR-33–deficient macrophages; their downstream effects might be responsible for the resolution of PF via an increase in autophagy, decrease in apoptosis, amelioration of the inflammation, and improvement of mitochondrial homeostasis. The gene discussed is PPARGC1A; the disease is pemphigus foliaceus.