Although analyses in the UK ALL2003 trial showed that an activation of IL7R-JAK did not confer an adverse prognosis in T-ALL [50], in vitro analysis of steroid resistance showed an association of IL7R-JAK-STAT mutations with a strong activation of the downstream oncogenic MEK-ERK and AKT pathways; thereby inducing a robust antiapoptotic response by upregulating MCL1 and BCLXL expression [49]. This evidence concerns the gene BCL2L1 and acute lymphoblastic leukemia.