As IGF2 and insulin exhibited much less efficacy (Figure 2A,B), IGF1 likely stimulated OPC‐like TICs through the IGF1R.[33] This conclusion is supported by that small molecule IGF1R inhibitors (Figure S4B–G, Supporting Information), CRISPR‐Cas9 (Figure 2N–P), shRNA (Figure S4H,I, Supporting Information), and MicroRNA (Figure S4J–M, Supporting Information)‐based genetic approaches could effectively suppress the growth of tumor OPCs stimulated by IGF1/2. The gene discussed is IGF1R; the disease is neoplasm.