Reexpression of CK1α or IRF4 rescues PEL cells from IMiD-mediated toxicity. (A) Representative western blots of BCBL-1 cells transduced with constitutive lentiviral vectors expressing GFP, WT, or G40N CK1α. Cells were treated for the indicated duration with 1 µM of pomalidomide. The asterisk in the anti-CK1α blot marks a nonspecific band. GAPDH served as loading control. (B) Pomalidomide IC₅₀ values of BCBL-1 cells analyzed in panel A (n = 3; error bars represent standard error of the mean [SEM]). (C) Representative western blots demonstrate efficient loss of endogenous, but not exogenous, IRF4 expression after treatment with 1 µM of pomalidomide. GAPDH served as loading control. (D) Pomalidomide IC₅₀ values of naïve BC-3 and BCBL-1 and cell lines transduced with a Dox-inducible IRF4 expression vector (n = 3; error bars represent SEM). (E) Pomalidomide IC₅₀ values of naïve BCBL-1 cells and cell lines transduced with a Dox-inducible IRF4 expression vector and constitutive lentiviral vectors expressing ZsGreen or G40N CK1α (n = 3; error bars represent SEM). (F) Representative western blots for IRF4 and CK1α of cells analyzed in panel E. The dotted line indicates where the image was cropped to remove irrelevant lanes. GAPDH served as a loading control. *P < .05, **P < .01, ***P < .001 by unpaired t test.