Furthermore, genetic knockout of PTPN11 in tumor cells enhanced MHC class I expression in co-culture, while the exogenous expression of the drug-resistant SHP2 mutant in tumor cells failed to upregulate tumor MHC class I levels upon SHP099 treatment (Fig. 5d and Supplementary Fig. 7b), thereby confirming that the enhanced IFNγ signaling in the cancer cells by SHP099 is due to on-target inhibition of SHP2. This evidence concerns the gene PTPN11 and neoplasm.