Proton therapy efficiency can be described as the ratio between tumour and non-tumour dose, while the tumour receives the planned dose. This efficiency is limited by the energy deposition property of the proton. To enhance the efficiency beyond this physical limit, targeted nuclear reactions during proton therapy could be exploited. For this purpose the 11B(p,3a) reaction has been researched. The three alpha particles created have a high linear energy transfer (LET) and cause an increase in energy deposited at the reaction site. This reaction has a high cross section for low proton energies and protons have a low energy in the tumour area. Hence, proton 11B capture will more frequently occur in the tumour area, which can increase the tumour to non-tumour dose. Proton boron capture therapy (PBCT) has been studied, using Monte Carlo simulation and by conducting experiments, which suggested a 90 and 50% increase in energy deposited respectively. However, these results were contradicted by other research, stating the 11B(p,3a) reaction could not significantly increase energy deposited during proton therapy. This discussion formed the foundation of this thesis. Two Monte Carlo methods, MCNP6 and Geant4, were used to investigate the reproducibility of the results obtained in previous research. First, MCNP6 simulations were done, which did not result in significant dose increase for proton therapy. To investigate the reproducibility of MCNP6 a second Monte Carlo method, Geant4, was used. Geant4 simulations produced similar results to MCNP6, equally not reproducing the promising results of previous research. Neither Monte Carlo method included all possible reaction cross sections for alpha particle creation during PBCT. Therefore, a simple Boltzmann model was made to simulate proton and alpha particle transport, including these missing reaction cross sections. To simulate the effect of below 1 MeV proton boron capture, a non-dynamic Boltzmann model was used, which resulted in a non significant increase in alpha production during PBCT. Afterwards, an alpha-proton-alpha avalanche reaction was investigated. For the effects of this reaction to be investigated a dynamic Boltzmann model was used, which resulted in no significant increase in alpha production either. To investigate if the 11B(p,3a) reaction could cause the increase in cell death found by experimental work, the cell killing potential of each alpha particle created was calculated analytically. Using the alpha production rate from the non-dynamic model, this calculation resulted in ten cells killed per alpha particle created. The alpha particles created during PBCT have a track length similar to the size of one cell, therefore it is unlikely for an alpha particle to kill ten cell. None of the obtained results, provide evidence that the 11B(p,3a) reaction will enhance the efficiency of proton therapy. Thus, we hypothesize that the experimental results could be related to boron having a radio sensitizing effect on cells. To test this irradiating boronated cells with gamma rays is proposed as the next step for further research.