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A growth-deficiency phenotype in heterozygous mice carrying an insulin-like growth factor II gene disrupted by targeting

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Jesse Rowley and his colleagues from Utah, have attacked this problem for variants in the ITGA2B and ITGB3 genes in patients with Glanzmann thrombasthenia (GT) by adopting CRISP-Cas-mediated homology-directed repair (HDR) to reproducibly insert precise gene variants into human cord blood and adult CD34+ cell-derived megakaryocytes (MKs)

[3] [4] Effects on blood pressure are less clear