However, the p21 down-regulation in FLT3-ITD+ cells triggered by inhibitors of FLT3-ITD, p53, PI3 kinase, and PKA suggests that the sustained inhibition of FLT3-ITD or other molecular pathways downstream of FLT3-ITD may block endogenous anti-growth signaling, possibly contributing to the recurrence of FLT3-ITD+ AML. Here, CDKN1A is linked to acute myeloid leukemia.