In pharmacological terms, our transgenic mouse model of MPN-like disease, when switched to dox containing diet, may mimic the actions of a V617F mutation-specific JAK2 inhibitor in the context of the heterozygous mutant clone, i.e. with one wild type JAK2 allele still being present: In the transgenic mouse model JAK2V617F expression is switchable in the background of wild type murine Jak2. Thus, when transgene expression is turned off, the cell’s Stat signaling relies again entirely on normal Jak regulation. Here, SOAT1 is linked to myeloproliferative neoplasm.