In comparison 1, 2.9% (2/68) and 3.9% (2/51) of TRs in MASTER 1 and the panel, respectively, were based on identical BMs, but resulted in different TRs (Fig. 3a): In both cases, a stop-gain mutation in NF1 was used as a rationale for mTOR inhibition in MASTER 1, but served as the basis for MEK inhibition in the respective panel analyses, which were evaluated 43 and 59 months later, respectively, primarily due to new BM-stratified clinical data from other cancer entities (patients 1 and 6; Supplementary Data 2 and 4). The gene discussed is NF1; the disease is cancer.