Streptococcus pneumoniae (the pneumococcus) is a formidable human-adapted pathogen responsible for more than 1 million deaths annually. Colonisation of the nasopharynx is critical for pneumococcal pathogenesis. Carbon sources are scarce in this niche, meaning the pneumococcus must scavenge to utilise what is predominantly available - galactose. Galactose metabolism occurs via two pathways in the pneumococcus, the Leloir and the Tagatose-6-Phosphate (T6P) pathways. The primary of these is the Leloir pathway, which is governed by the galactose regulator GalR. GalR possesses three putative phosphorylation sites: S317, T319 and T323. A recent study from our group revealed that these putative phosphorylation sites play a critical role in both galactose metabolism and infection. Specifically, mutation of these sites to non-phosphorylatable alanine residues (D39AAA) resulted in shutdown of Leloir pathway gene expression, leading to a decreased ability to grow when galactose is the sole carbon source. A murine model of pneumonia infection also showed a decreased ability for D39AAA to persist in the nose, lungs and ears, compared to the wild-type D39 strain. We also uncovered a potential link between the Leloir and T6P pathways, with deletion of genes from either pathway resulting in an inability to metabolise galactose. More recently, we have revealed that the putative GalR phosphorylation sites play a critical role in progression of disease in mice, resulting in rewiring of the host immune response during infection of the lung. This study shows the critical importance of not only GalR, but its putative phosphorylation sites in S. pneumoniae, whilst highlighting the complexity of pneumococcal galactose metabolism. Gaining a greater understanding of the mechanisms underpinning pneumococcal colonisation of the nasopharynx creates new avenues for the exploration of novel methods to prevent colonisation and subsequently pneumococcal disease.