The ERCC6L2–TP53 paper strongly supports the idea that AML (especially TP53) is not just a mutation, but a dynamic stress and evolution problem. The disease is constantly evolving, not static.
This fits well with clinical data, where responses are achieved but OS remains at the 10-month level. Simply killing blasts is not enough; the microenvironment also likely plays a significant role in the duration of the response.
This paper includes Finnish researchers and Mikko Myllymäki, who was just on TV with Juho and is also involved in BEXMAB studies. Of course, this is not proof of anything, but it indicates that the same group investigating the core causes of AML is also involved in developing its treatment.