BTK and diffuse large B-cell lymphoma: As such, further evaluation of mechanisms derived from TP53 [62], SOCS1 [63], CD36 [64], BTK [65], or EZH2 [66] mutations in primary refractory DLBCL may shed light on disease driving mechanisms in these highly aggressive cases and present opportunities for more targeted second line therapy for those not eligible for ACST or CAR-T.