Dr Cahill studied Science at the University of New South Wales, graduating with BSc (Hons 1) in Zoology with a strong Biochemistry emphasis in 1987 and a PhD from the Department of Pathology, School of Medicine of the University of NSW, working on the transcriptional regulation of the c-fos gene as an external student based at the Medizinische Hochschule in Hannover, Germany. After finishing his doctoral thesis in late 1994 he remained in the same lab for another twelve months as a “post doctoral scientist” (postdoc) before moving back to Australia in late 1995.

Being interested in signal transduction events in the cytoplasm, he was captivated in 1996 by the then emerging field of proteomics; so much so that he moved from Canberra back to Germany where from 04/1997 to 01/2000 he established a proteomics laboratory as postdoc/group leader at the University of Tuebingen. That activity later developed into the present Tuebingen Proteomics Centre. However before that centre was officially opened he had left the academic world to co-found a proteomics-based biotechnology company called ProteoSys AG, based in Mainz. There he remained as Chief Research Officer until 2007, after which he ‘moved back home’ to re-enter academic life in Australia. Dr Cahill commenced as a biochemistry lecturer at CSU in Wagga Wagga in 2008. Durign his time at CSU he served at different times as School Honours Coordinator, Chair of the School Research Committee, and as an elected staff representative serving on both Academic Senate and the CSU Research Committee. He taught in the areas of nutritional metabolism, biochemistry, molecular cell biology, and genomics, proteomics and bioinformatics. Dr. Cahill chose to cease employment with CSU in January 2021, and has been an adjunct academic since then. Since 2019 Dr. Cahill has also been an honorary Senior Lecturer at the Australian National University.

Dr. Cahill's research interests cover the healthy and pathological biology of the cell signalling system surrounding the protein "Progesterone Receptor Membrane Component 1". He has recently shown that PGRMC1 phosphorylation is involved in mitochondrial morphology and metabolic function, and in epigenetic gene regulation that drives cell phenotypical plasticity. PGRMC1's phosphorylated tyrosines appeared in evolution at the same time as the gastrulation organiser and derived specialised cell types, such as neurons. We are begining to understand the broad range of effects of PGRMC1 in diseases like cancer (Warburg effect metabolism) and neurodegeneration. For instance, it is emerging that Alzheimer's disease may be caused by perturbations in PGRMC1 function, which cause all of the downstream effects commonly researched (amyloid beta, Tau. ApoE, epigentics, glucose metabolism, and mitochondrial dysfunction). The future will attest whether these unorthodox statements bear the test of time (no other Australian Alzheimer's researcher would argue this). Dr. Cahill is confident that it will be so.