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<i>Fusarium verticillioides</i> produces fumonisins, which are mycotoxins inhibiting sphingolipid biosynthesis in humans, animals, and other eukaryotes. Fumonisins are presumed virulence factors of plant pathogens, but may also play a role in interactions between competing fungi. We observed higher resistance to added fumonisin B₁ (FB₁) in fumonisin-producing <i>Fusarium verticillioides</i> than in nonproducing <i>F. graminearum</i>, and likewise between isolates of <i>Aspergillus</i> and <i>Alternaria</i> differing in production of sphinganine-analog toxins. It has been reported that in <i>F. verticillioides</i>, ceramide synthase encoded in the fumonisin biosynthetic gene cluster is responsible for self-resistance. We reinvestigated the role of <i>FUM17</i> and <i>FUM18</i> by generating a double mutant strain in a <i>fum1</i> background. Nearly unchanged resistance to added FB₁ was observed compared to the parental <i>fum1</i> strain. A recently developed fumonisin-sensitive baker’s yeast strain allowed for the testing of candidate ceramide synthases by heterologous expression. The overexpression of the yeast <i>LAC1</i> gene, but not <i>LAG1</i>, increased fumonisin resistance. High-level resistance was conferred by <i>FUM18</i>, but not by <i>FUM17</i>. Likewise, strong resistance to FB₁ was caused by overexpression of the presumed <i>F. verticillioides</i> “housekeeping” ceramide synthases <i>CER1</i>, <i>CER2</i>, and <i>CER3</i>, located outside the fumonisin cluster, indicating that <i>F. verticillioides</i> possesses a redundant set of insensitive targets as a self-resistance mechanism.