A mutual crosstalk between growth factors acting through receptor tyrosine kinases (RTKs) of ERBB family and steroid hormones acting through nuclear receptors (NRs) is attained by both genomic and non-genomic interactions.

Steroid hormones fine-tune ERBB signalling dynamics and cellular output by modulating feedback regulatory loops.

Drug combinations of NR and RTK agonists or antagonists may be a strategy for the development of new therapies in a broad range of diseases, including cancer.

Understanding the circadian glucocorticoid regulation of ERBB (and RTK) signalling provides the basis for chronotherapy to improve anti-cancer treatment efficacy.

Time-resolved analysis of the global genomic response to steroid hormones and growth factor combinations could lead to major advances in molecular medicine.