In vitro studies demonstrated the interconnection between these two pathways, since stimulation with TSLP, which is the CRLF2 ligand, induced phosphorylation of both JAK/STAT and PI3K/Akt/mTOR pathway components, while treatment with the JAK inhibitor Ruxolitinib inhibited the activation of STAT5, ERK1/2 (downstream JAK/STAT signaling), Akt, S6RP, 4EBP1, and eIF4E (downstream PI3K/Akt/mTOR signaling), in both cell lines and primary samples from ALL patients [109]. This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.