Recent comprehensive genetic analyses of t(17;19)‐ALL and t(1;19)‐ALL using patient‐derived xenografts revealed significant differences between the molecular landscape of the two groups; deletions of PAX5 and VPREB1 and mutations of TCF3 and RAS pathway genes such as NRAS, KRAS, and PTPN11 were more frequently observed in t(17;19)‐ALL samples.17 These observations suggest an unconfirmed possibility that these additional genetic abnormalities may be involved in the poor therapeutic response of t(17;19)‐ALL in association with TCF3‐HLF. Here, KRAS is linked to acute lymphoblastic leukemia.