Step 1: This is a negative-stem question, so three statements are correct facts about sunitinib and we must spot the single error.
Step 2: Sunitinib acts on many tyrosine kinase receptors at once, dampening signalling through VEGFR, PDGFR and c-kit. This broad blockade underlies its antitumour effect, confirming the receptor-inhibition statement.
Step 3: Tumours driven by these pathways respond well. Renal cell carcinoma leans on VEGF-mediated angiogenesis, and GIST is driven by c-kit and PDGF signalling, so the drug is a recognised therapy for both. Those two clinical statements hold true.
Step 4: Where the question trips you up is excretion. The drug undergoes hepatic metabolism and leaves the body chiefly in the stool rather than the urine. The claim of primary urinary excretion is therefore wrong.
\[\boxed{\text{It is excreted primarily in urine}}\]