Several mechanisms have been identified as immune pressure inducing a lineage switch from ALL to a myeloid phenotype that occurs in MLL-rearranged B-ALL [8], including homozygous mutations of the B cell receptor protein complex [9]; splicing or mutations, respectively, of the CD19 mRNA or gene [10–12]; and tumor/CAR T cell membrane exchange that decreases antigen density and induces fratricidal CAR T cell killing (trogocytosis) [13]. The gene discussed is CD19; the disease is neoplasm.