Lenvatinib sustains anti-angiogenic pressure via VEGFR1–3 and FGFR1–4 but does not inhibit RAF, a profile that in trials and reviews aligns with a toxicity pattern dominated by hypertension, proteinuria, and gastrointestinal effects, with less prominent HFSR than RAF-inhibiting MKIs (39–42); this difference explains the improved cutaneous tolerability we observed. The gene discussed is FLT1; the disease is hypertensive disorder.