As part of the adaptive immune system, T cells are vital for the eradication of 
infected and malignantly transformed cells. To perform their protective 
function, T cells produce effector molecules that are either directly cytotoxic, 
such as granzymes, perforin, interferon-γ and tumour necrosis factor α, or 
attract and stimulate (immune) cells, such as interleukin-2. As these molecules 
can also induce immunopathology, tight control of their production is required. 
Indeed, inflammatory cytokine production is regulated on multiple levels. 
Firstly, locus accessibility and transcription factor availability and activity 
determine the amount of mRNA produced. Secondly, post-transcriptional 
mechanisms, influencing mRNA splicing/codon usage, stability, decay, 
localization and translation rate subsequently determine the amount of protein 
that is produced. In the immune suppressive environments of tumours, T cells 
gradually lose the capacity to produce effector molecules, resulting in tumour 
immune escape. Recently, the role of post-transcriptional regulation in 
fine-tuning T-cell effector function has become more appreciated. Furthermore, 
several groups have shown that exhausted or dysfunctional T cells from cancer 
patients or murine models possess mRNA for inflammatory mediators, but fail to 
produce effector molecules, hinting that post-transcriptional events also play a 
role in hampering tumour-infiltrating lymphocyte effector function. Here, the 
post-transcriptional regulatory events governing T-cell cytokine production are 
reviewed, with a specific focus on the importance of post-transcriptional 
regulation in anti-tumour responses. Furthermore, potential approaches to 
circumvent tumour-mediated dampening of T-cell effector function through the 
(dis)engagement of post-transcriptional events are explored, such as 
CRISPR/Cas9-mediated genome editing or chimeric antigen receptors.