Interestingly, mTOR was reported to directly upregulate STAT3 activity by enhancing its phosphorylation at the S727 residue.23 Alternative approaches, including JAK and mTOR inhibition, could suppress STAT3 activity and function as therapeutic methods for lymphoproliferative disorders caused by constitutive STAT3 activation.24 In our study, we explored the activation state of possible factors involved in the JAK2/STAT3 pathway and found that DCZ0858 inhibited the phosphorylation of PI3K, Akt, and mTOR, which most likely contributed to the observed antitumor effects. This evidence concerns the gene STAT3 and lymphoproliferative syndrome.