The temperature dependence shown in two independent alleles of mua-3 is interesting. Despite the wide use of temperature-sensitive (ts) mutations, especially for studying essential genes that cause lethality when they are deleted, the molecular basis of ts phenotypes is largely unknown. It is generally assumed that the lethality results from thermal inactivation of gene products. However, there are also several lines of evidence suggesting that the exacerbated phenotypes at the nonpermissive temperature come from the changes in conditions under which the molecules function that coincide with the temperature shift (Van Voorhies and Ward 1999; Masuda et al. 2013), such as rates of metabolism or development processes. Our result that a null mutation of dbl-1 has different body size depending on temperature also supports this idea. Therefore, higher temperature may exacerbate mua-3 phenotypes by increasing metabolic rate and/or by speeding the developmental processes. One of the current treatments for Marfan syndrome is β-adrenergic blockers that lower heart rate and slow aortic growth. However, this only ameliorates the deleterious symptoms of progressive aortic root enlargement and aortic dissection. If metabolic rate plays any role in regulating disease progression, then a combined treatment with β-adrenergic blockers and a drug that decreases metabolic rate may help further to alleviate Marfan syndrome.