Step 1: Identify the target organ. Acne begins in the sebaceous (oil) gland, and the gland that is exquisitely sensitive to androgenic hormones.
Step 2: Link hormone to effect. Testosterone is converted in the skin to dihydrotestosterone, which drives excess sebum secretion and plugging of follicular openings, producing comedones that progress to inflammatory papules and pustules.
Step 3: Clinical correlation. Acne classically erupts at puberty when androgen levels rise and worsens in hyperandrogenic conditions, confirming testosterone as the culprit.
Step 4: Rule out alternatives. Estrogen suppresses sebaceous activity (basis of hormonal acne therapy), thyroid hormone is unrelated, and gonadotropins influence acne only by way of stimulating androgen production, not directly.
\[\boxed{\text{Testosterone}}\]