At present, as a means to circumvent a subset of glucocorticoid (GC)-associated side effect, the focus of my work not only includes the unravelling of fundamental Glucocorticoid receptor (GR)-mediated transrepression mechanisms but also includes a mechanistic study of non-steroidal dissociated GR ligands.

Apart from this, I study the applicability of another way of skewing therapeutic responses towards a more desirable profile, by using dual nuclear receptor triggering. This involves combination schemes using GR agonists combined with Peroxisome Proliferator-Activated Receptor (PPAR) agonists.