In general, successful Nucleofection® is vector independent, with one important caveat. Some expression plasmids utilize promoters and enhancers obtained from the Long Terminal Repeats (LTR's) of retroviruses, and when these expression plasmids are transfected into cells by Nucleofection®, the expression of the cloned genes is suppressed by the cell. 
Although the mechanism of suppression is not known, we have certain ideas on what might be happening. Since with Nucleofection®, the DNA is introduced immediately into the nucleus, if there are viral elements present in the transfected DNA, the cell can be tricked into responding as if this were a viral invasion, and move to suppress the expression of the DNA, presumably through DNA methylation.
This is particularly true in primary cells, which have all of the normal cellular self-defense mechanisms still intact, and is true to a lesser extent with cell lines. During the process of immortalization or transformation, many cell lines lose parts their DNA surveillance mechanisms that normally protect the cell. Depending on which parts of these mechanisms are lost, cell lines may or may not be able to suppress the expression of cloned genes driven by retroviral LTR-based promoters. Therefore, if the expression plasmid contains promoters or enhancers derived from retroviral LTR's, it is likely that these plasmids will not function well in primary cells and some cell lines. The only effective alternative is to reclone the gene of interest into a different expression plasmid that uses conventional promoters such as CMV, EF1a, SV-40, or similar promoters.