The lack of a complete response in MPN patients treated with ruxolitinib might be due to the activation of collateral oncogenic pathways, like the one of c-Jun N-terminal kinase (JNK) or PI 3-kinase (PI3K)/AKT serine/threonine kinase (AKT)/ mammalian target of rapamycin (mTOR) pathway [45]. Here, AKT1 is linked to myeloproliferative neoplasm.