In fact, B-ALL cells unable to signal through the IFNγR/JAK/STAT pathway were functionally deficient for Qa-1b suggesting that the mechanism by which IF IFNγR/JAK/STAT signaling promotes CAR-T resistance is, at least in part, dependent on IFNγ-induced Qa-1b surface expression on tumor cells. Here, SOAT1 is linked to neoplasm.