Pathophysiologic mechanisms often mirror the therapeutic action: immunotherapies (CAR T, ICIs, bispecifics) tend to cause inflammatory or immune-mediated ocular conditions (uveitis, optic neuritis, etc.), whereas targeted drugs that inhibit signaling pathways (TKIs) cause ocular effects related to those pathways’ roles in ocular tissues (e.g. PDGFR inhibition causing edema, or off-target kinase inhibition causing epithelial dysfunction). This evidence concerns the gene PDGFRB and optic neuritis.