We propose that ICT exerts its multi-target anti-HCC activity through synergistic mechanisms—inhibiting CA9 (microenvironment regulation), UCK2 (nucleotide metabolism), and FABP5 (lipid metabolism), while enhancing CYP2C9 expression, which collectively contribute to its potent antitumor efficacy. The gene discussed is CYP2C9; the disease is hepatocellular carcinoma.