Novel treatment strategies for T-PLL are urgently needed; candidate agents in clinical development for T-PLL include anti-BCL2 (alone 9 or in combination with ibrutinib [NCT03873493]), JAK/STAT pathway inhibitors (eg, combined tofacitinib and ruxolitinib, 10 or itacitinib [NCT03989466]), and anti-histone deacetylase (eg, romidepsin [NCT02512497]). In this scenario, the availability of robust diagnostic criteria, well-established indications for treatment, and homogeneous responses represent essential tools for investigating these novel therapies. Furthermore, the systematic investigation of biological features associated with disease progression may lead to the identification of molecular targets for the development of novel therapeutic agents. Future investigations are needed to validate these criteria and to identify baseline characteristics and longitudinal indicators associated with better long-term outcomes. Hopefully, this will also lead to the identification of meaningful clinical end points that may help assess the possible impacts of novel treatments. Indeed, we need to understand whether complete remission is required for long-term survival, or if even partial remission could result in satisfactory progression-free survival, especially in the era of novel, continuously given, target therapies. In contrast, if complete remission is the initial treatment goal, we will need to understand the meaning of minimal residual disease and its role in driving therapeutic interventions for subsequent maintenance or consolidation treatments. Of course this work from the TPLL-ISG is not the end of the story, but rather a starting point that paves the way for future clinical investigations that will improve the treatment of patients with T-PLL.