The fundamental mechanism of androgenetic alopecia (AGA) is the depletion of the anagen phase causing clinical presentation of hair miniaturization. The imbalance of autophagy signaling led to a reduction of the anagen phase and an increase in senescence of dermal papilla (DP). FoxO3a, one of the upstream autophagy-regulated proteins, has been well studied in many cell types and relevant diseases. However, the function of FoxO3 and its relevant role in the autophagy mechanism becomes a mysterious phenomenon in hair regeneration and AGA. We randomly recruited multiple bulge areas of the outer root sheath from 10 tissue sections for each staining biopsied from 2 healthy volunteers and 3 early-onset androgenetic alopecia patients. Here, we aim to study FoxO3a expression by comparing early-onset AGA to normal. 5-μm formalin-fixed paraffin-embedded (FFPE) vertical sections of biopsiedscalp samples were used in immunohistochemical (IHC) assays and assessed scoring using Qu path software. The FoxO3a, S253 phosphorylated FoxO3a, and 14-3-3 were significantly identified in the bulge area of the outer root sheet of the disease group with a higher positive intensity of IHC staining in the AGA group than the normal at 12.7 %, 23.8 %, and 0.7%, respectively. Interestingly, increased phosphorylated FoxO3a and 14-3-3 protein expression in the AGA group possibly demonstrated the loss of nuclear localization that was eventually lost to transcriptional factor activities encoding autophagy-related genes. These illustrated the clinicopathological significance of early-onset AGA and the imbalance in cell signaling of the protein involved in autophagy.