Germline mutations in components of the Ras/MAPK signaling pathway result in developmental disorders called RASopathies, affecting ~1/1000 human births. Advances in genome sequencing are making it possible to identify disease-related mutations, but currently there is no framework for patient-specific predictions of disease progression based on the individual mutations. Here, we focus on all 14 MEK1 mutations found in RASopathies as well as 2 MEK1 mutations found only in cancer. We find that these can be robustly ranked according to their effect on oval shape of the zebrafish embryo at 11 hours post fertilization (hpf) and lethality fraction at 48 hpf using a quantitative, but also quick and inexpensive approach of MEK1 variant overexpression by microinjection of mRNA at the 1-cell stage. We found that mutations identified in cancer were stronger than those identified in both RASopathies and cancer, which, in turn, were generally stronger than those identified only in RASopathies. We also find that this rank extends to heart size at 20 hpf in zebrafish, another Ras/ERK-dependent developmental process. Moreover, this rank is conserved in other fly-specific assays including ectopic wing vein formation and lethality fraction. Finally, we show that this rank is predictive of MEK inhibitor dosages needed to reverse the oval shape defect, although there is a balance between correcting a particular defect fully and altering other Ras/ERK-dependent developmental processes. These assays can be used to test the strength of newly found MEK1 mutations as well as for RASopathy and cancer mutations in other pathway components.