Early trials primarily evaluated small-molecule monotherapies, often targeting the renin-angiotensin system to inhibit angiotensin-driven HSCs activation and collagen synthesis—this strategy aligned with contemporaneous etiological contexts such as hepatitis C and resonated with the proliferation of A61K31/patents, where high-frequency filings directly propelled the clinical dominance of small-molecule candidates. This evidence concerns the gene REN and hepatitis C virus infection.