AMFR and VEXAS syndrome: Interestingly, AF potently enhanced gp78-catalyzed ubiquitination in the presence of the cytosolic form of UBA1, UBA1b, or the VEXAS syndrome-causing UBA1c, a truncated form of UBA1b that uses methionine 67 as translation start codon due to mutations of codon methionine 4115 (Fig. 5b, c).