Within this context, PTPRG has unique features as it is specifically downregulated in CML and has been demonstrated to have a functional role being capable of binding and dephosphorylating the driving oncoprotein BCR-ABL1 and consequently reducing total and specific phosphotyrosine levels as well as clonogenic capacity in various CML cells [8]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.