The introduction of immune checkpoint inhibitors (ICIs) has drastically improved metastatic melanoma patient outcomes. Unfortunately, varied therapeutic response rates and the acquisition of resistance has limited therapeutic success. This has driven a new field of combination therapy, aimed at targeting mechanisms of resistance, and generating immunostimulatory responses – but current strategies remain largely ineffective. Bortezomib (BTZ), a 26S proteasome inhibitor utilised in several cancer types, induces immunogenic anti-tumour responses via a specific ER stress-induced apoptotic cell death pattern, known as Immunogenic Cell Death (ICD). Whilst BTZ has been shown to be ineffective as a systemic monotherapy for melanoma, the opportunity of repurposing the drug for combination with ICI remains a potentiality. We demonstrate that the combination of BTZ enhances ICI and clears disease in a subset of mice whilst showing little response in others. The mechanism of BTZ immunogenicity and deviation in responders remains unclear and must be investigated. We aimed to assess the impact of BTZ on tumour responses in vitro and investigate a potential cell cycle role in immune evasion after BTZ treatment. Three well-established human metastatic melanoma cell lines were transduced with a Fluorescent-Ubiquitination Cell Cycle Based Reporter system (FUCCI), which allowed for investigation into a cell cycle-dependent role of potential evasion after BTZ treatment. Flow cytometric analysis indicated a time-dependent increase in HLA-I expression after BTZ treatment in multiple metastatic human melanoma cell lines. Stratification to cell-cycle phase revealed a preferential increase of HLA-I in G1-phase cells. These findings highlight a potential mechanism of enhanced anti-tumour CD8+ responses and support a synergistic combination with ICI therapy.