Upregulation of IGF1R activity is capable of promoting EMT, cell invasiveness, and motility through positively modulating numerous signaling effectors, e.g., Src and STAT3.6 Given an increase in IGF1R autophosphorylation upon MTAP loss, we treated RCC cells with the selective IGF1R inhibitor linsitinib (OSI-906) to pharmacologically block IGF1R autophosphorylation and activation of the downstream signaling proteins.11 As shown in Fig. 5a (left), MTAP KO cells displayed higher levels of protein tyrosine phosphorylation than did WT 786-O cells. The gene discussed is IGF1R; the disease is renal cell carcinoma.