Cellulose is an important structural molecule in the plant cell wall. Recently, the receptor-like kinases FEI1 and FEI2 were found to regulate cellulose synthesis. When grown on high sucrose media, the fei1fei2 double mutant has short, swollen roots due to cellulose deficiency. The phytohormone ethylene is known to inhibit root elongation, thus causing root growth defects. The fei1fei2 phenotype is not reverted to wild-type when ethylene perception is disrupted, indicating that ethylene is not involved in the FEI pathway. However, a reversion of the fei1fei2 phenotype has been observed when ethylene biosynthesis is inhibited. In the ethylene biosynthesis pathway, 1-aminocyclopropane-1-carboxylic acid (ACC) is the direct precursor to ethylene. This, together with other genetic and biochemical studies, suggests that ACC acts as a signal in the FEI pathway. We have found that the ethylene-insensitive line, ein2-5, responds to the application of ACC but not ethylene, suggesting that ACC signals independently of ethylene. Additionally, ACC reestablishes swelling in fei1fei2ein2-5 mutants in which ethylene biosynthesis has been inhibited. Here, we examined the role of ACC in cellulose biosynthesis to confirm the biochemical effects of ACC in the FEI pathway. To do so, we genetically and physiologically disrupted ethylene biosynthesis and signaling in a fei1fei2 background. Our findings on the role of ACC in the FEI signaling pathway and thus cellulose synthesis will likely impact industry, where understanding cell wall composition may lead to enhanced production of cellulose-based goods such as paper and biofuels.