Another potential mechanism is that gut microorganisms might modulate the tumour immune microenvironment – in anti-PD-1 responders, a significant correlation was found between baseline CD8+ T cells in the TME and the abundance of Faecalibacterium genus, Ruminococcaceae family and Clostridiales order, suggesting these microorganisms may promote the development of a hot TME, whereas a negative association was seen with Bacteroidales [78]. The gene discussed is CD8A; the disease is neoplasm.