The evolutionary dynamics of complex traits is constrained by levels of genetic variation as well as genetic correlations among traits. Because the ultimate source of all genetic variation is mutation, the distribution of mutations entering populations profoundly affects standing variation and genetic correlations. I will present results from a recent joint study with Adam Jones and Stevan Arnold of an individual-based quantitative genetic model that was designed to investigate how natural selection and gene interactions (i.e., epistasis) shape the evolution of mutational processes affecting complex traits. We found that the presence of epistasis allows natural selection to mold the distribution of mutations, such that mutational effects align with the selection surface. Consequently, novel mutations tend to be more compatible with the current forces of selection acting on the population. Counterintuitively, we found that smaller populations can sometimes harbor higher genetic variances than corresponding larger ones. The reason is that evolved mutational variances are inversely related to population size. These results suggest that in many cases mutational effects should be seen as an outcome of natural selection rather than as an unbiased source of genetic variation that is independent of other evolutionary processes.