SP1 and precursor B-cell acute lymphoblastic leukemia: Here we uncovered that depletion of β-Arrestin1 enhanced cell senescence of B-ALL LICs in vivo and in vitro by regulating the hTERT-telomerase-telomere axis through inducing P300-Sp1 interaction at the −28 to −36 bp region of hTERT promoter, and decreased senile cells and elevated expression of β-Arrestin1 predicted poor prognosis in B-ALL.