IGF1R and neoplasm: Compared with IGF1R overexpression alone, activation mutations at Y1165/1166 further diminished the inhibitory effect of surufatinib on tumor growth, whereas inactivation mutations at these sites reduced tumor burden and rendered tumors more responsive to surufatinib treatment (Fig. 3L–N), underscoring the critical role of IGF1R Y1165/1166 phosphorylation in determining surufatinib sensitivity.