An interesting exception to the in vitro and in vivo opposing phenotypes witnessed among regulators in response to CAR-T therapy was Ptpn2. PTPN2 is a negative feedback regulator of IFNγR/JAK/STAT signaling; loss of PTPN2 leads to sustained IFNγR/JAK/STAT signaling, and drugs to inhibit PTPN2 and amplify tumor responses to checkpoint blockade are in clinical development42. This evidence concerns the gene SOAT1 and neoplasm.