A universal feature of the membranes that form the boundary of all cells is their capacity to permit the transfer of both chemical entities and information. Critical to the latter are trans-membrane receptors, of which the receptor tyrosine kinase family form a particularly important category in the context of regulating growth and proliferation. Through being able to respond to ligand binding by stimulating multiple pathways of intracellular proteins, activated receptors signal to the nucleus to regulate gene expression. Components of these pathways, including the receptors themselves, are frequently mutated in cancers, giving rise to aberrant proliferation control. To illustrate the principles of signalling we will consider one major example: the RAS-MAPK pathway activated by epidermal growth factor (EGF) through its receptor (EGFR), a member of the receptor tyrosine kinase family. The critical result of such signalling is the activation of transcription of key genes required for cells to enter the division cycle, a master regulator being MYC. Steroid hormones that diffuse across membranes before binding to their receptors also play significant roles in cancer and modulation of their effects has been an important therapeutic strategy.