Introduction: Chronic mucocutaneous candidiasis(CMC) is characterised by recurrent or persistent Candida infections of the skin, nails and mucous membranes, and is frequently associated with underlying inborn errors of immunity . The diagnosis of CMC requires genetic confirmation; therefore, it is challenging in resource-limited settings. Case presentation: A 16-month-old boy , the third-born child of non-consanguineous parents with no significant family history , presented with recurrent oropharyngeal candidiasis since 8 months of age. Despite repeated courses of topical and systemic antifungal therapy , his clinical response had been suboptimal. On examination, he was undernourished and had extensive oral candidiasis, nail dystrophy and features of bronchopneumonia. Inflammatory markers were elevated, and chest radiography confirmed bronchopneumonia. He was treated with fluconazole along with broad-spectrum intravenous antibiotics. Due to treatment-resistant candidiasis and poorly resolving pneumonia, an underlying immunodeficiency was suspected. Secondary causes of immunodeficiency were excluded.Flow cytometry demonstrated mild natural killer (NK) cell deficiency with otherwise normal immune parameters. Upper gastrointestinal endoscopy revealed oral and extensive oesophageal candidiasis with involvement of the stomach and duodenum. Based on the clinical presentation, chronic mucocutaneous candidiasis was suspected. Whole exome sequencing identified a heterozygous gain-of-function mutation in the STAT1 gene, confirming the diagnosis of CMC. Conclusion: Persistent or recurrent treatment-refractory candidiasis beyond infancy should prompt evaluation for inborn errors of immunity . Early genetic diagnosis of STAT1 gain-offunction mutation-associated CMC is important to guide long-term management and surveillance for systemic complications.