Notably, despite the loss of GOLGA7 disrupting NRAS anterograde trafficking and resulting in its cis‐Golgi accumulation,[31] NRAS can signal from Golgi endomembrane to some extent,[43] such that all those NrasG12D/G12D; Mx1‐Cre+; Golga7KO mice ultimately developed CMML‐like MPN. The gene discussed is MX1; the disease is myeloproliferative disorder.