Mechanistically, loss of SH2B3 increases Janus kinase-signal transducer and activator of transcription signaling, promotes lymphoid cell proliferation, and accelerates leukemia development in a mouse model of NOTCH1-induced ALL.
Moreover, expression of Notch1, an essential gene for developing hematological cells and T-ALL, was found to be negatively correlated with β-arrestin1 in ALL.