Hematological malignancies associated with "ETY6" gene fusions to other transcription factor genes appear to reflect a loss or gain in function of "ETV6" and/or the other genes in regulating expression of their target genes; this results in the formation or lack of formation of products which influence cell growth, proliferation, and/or survival. In vitro studies of "ETV6-RUNX, ETV6-MN1, ETV6-PER1", and "ETV6-MECOM" fusion genes support this notion. Thus, the "ETV6-MECOM" fusion gene is overexpressed because it is driven by the promoter derived from "ETV6" whereas the "ETV6-RUNX, ETV6-MN1", and " ETV6-PER1" fusion genes produce chimeric proteins which lack ETV6 protein's gene-suppressing activity. The chimeric protein products of "ETV6" gene fusions with "ARNT, TTL, BA22A, FCHO2, MDS2", and "CHIC2" likewise lack ETV6 protein's transcription factor activity. Gene fusions between "ETV6" and the homeobox gens (i.e. "CDX2, PAX5," and MNX1) produce chimeric proteins with lack either ETV6s and/or CDX2s, PAX5s or MNX1s transcription factor activity. In all events, hematological malignancies associated with these fusion genes have been treated with standard chemotherapy protocols selected on the basis of the malignancies phenotype.