Combination therapy could a fast(er) road towards improving tumour response to treatment. The conference started keynote lecture Anthony Letai Harvard University discussing the importance of apoptotic priming for cancer sensitivity chemotherapeutic agents. Since decreased via mitochondrial pathway seems characterise multidrug-resistant relapsed tumours made compelling argument need strategically combine therapies in clinical practice 1-4. Other talks world-renowned researchers offered further support that such combinations benefit For instance his talk Jean-Emmanuel Sarry highlighted potential targeting oxidative phosphorylation sensitise cells suggests treating cytarabine resistant Acute Myeloid Leukemia combination venetoclax/ surpass resistance as venetoclax BCL2-selective inhibitor decreases stress and primes caspases-dependent apoptosis 5. Sandra Demaria Weill Cornell Medicine discussed benefits combining radiotherapy immune-checkpoint therapy. According Demaria DNA damage induced by can lead displacement fragments cytosol which will activate tumoral tumour-infiltrating dendritic innate adaptive immune responses normally triggered viruses (e.g cGAS/STING pathway). This leads increased inflammation attracts T hence facilitating checkpoint inhibitor 6-8. Sophie Pastel-Vinay brought evidence role immunogenicity. Vinay showed increasing through acting on pathway PARP inhibitors potentiate effect anti-PD-1 ERCC1-defective Non-Small Cell Lung Cancer BRCA1-defective triple-negative breast 9 10. Hormonal is not all bad news During conference progesterone receptors was highlighting risks hormonal treatments cancer. In Jason Carroll molecular crosstalk between oestrogen receptor pathways modulate binding chromatin. also debunked some findings WHI hormone trials conducted early 2000 suggesting may outcome risks at least when it comes went present PIONEER phase 2 trial combines standard-of-care antagonists letrozole agonists megace order treat changing activity 11. On other hand Cathrin Brisken’s research combined treatment enhance metastatic spread abrogation therapeutic option patients 12. These however do contradict Carroll’s but rather brings us highlight #3 There’s an personalised her presentation about cancer Brisken proliferative administration are patient-specific 12 13. presentation personalise based patient's profile. Microbiota influences development Maria Rescigno explained how pro-tumorigenic gut microbiota translocate liver where forms pre-metastatic niche promotes recruitment 14. bacteria change growth rate infiltrates progression 15.  In Lisa Derosa microbiome immunotherapy range solid tumours including melanoma bladder renal lung impact antibiotics probiotics have