RP mutations could be of particular interest in this context, and it was shown that tumor cells harboring the T-ALL associated mutation Rpl10 R98S are highly sensitive to clinically used Jak-Stat inhibitors, due to high activation of this pathway promoted by uL16 R98S-containing ribosomes (as mentioned in previous sections) (43). The gene discussed is RPL10; the disease is acute lymphoblastic leukemia.