ANKRD26 and Thrombocytopenia: This was considered responsible for the thrombocytopenia in the absence of 5′UTR variants, as the authors demonstrated increased ERK phosphorylation with either an overexpression of both a full-length or a truncated ANKRD26, with missing ankyrin repats and preserved coiled-coil domains, through lentiviral injection of cDNA from the complex structural variant into primary human CD34+ HSPCs from healthy donors [12].