To investigate the role of GATA1s in DS AMkL, we used lentiviral shRNA to knockdown the GATA1 gene in a DS AMkL cell line, CMK, established from a 1-year-old DS boy with AMkL and harboring a mutated GATA1 gene.[17] shRNA lentiviral infection resulted in 59% and 30% decreased levels of GATA1s in two clones, designated CMK-5a and -5b, respectively, compared to a pool of cells from the negative control infection (designated CMK-neg, Fig. 1A). The gene discussed is GATA1; the disease is infection.