AP-1 factors regulate the expression of CCND1 and E2F, which in turn regulates E2F-downstream genes, leading to the modulation of cellular proliferation, differentiation, apoptosis, oncogene-induced transformation, and cancer cell invasion.[38] While further studies are required to characterize the molecular mechanisms involved, our results strongly suggest that RP11-137H2.4 expression abrogates normal GC response in pre-B cALL samples by modulating the expression of MAPK cascade genes. This evidence concerns the gene CHL1 and cancer.