We have shown previously that SARIFA-positivity is likely the morphologic correlate of an underlying distinct tumor biology,13,14,17 characterized by a broad dysregulation of RNA expression exhibiting a partial overlap with CMS1 (microsatellite instability immune subtype) and CMS4 (mesenchymal subtype).14 As CMS1 is characterized by an impaired DNA mismatch repair (MMR) system as well as a high BRAF mutation rate,19 and CMS3 is﻿ characterized by an overrepresentation of K﻿RAS mutations,19 we hypothesized that SARIFA may be related to these clinically used molecular alterations. The gene discussed is BRAF; the disease is neoplasm.