Chimeric antigen receptor (CAR) T (CAR-T) cells represent a revolutionary treatment for haematological tumours but this success has not been extrapolated to solid tumours. Activation and expansion of transferred cells in vivo are key for the success of CAR-T therapy, with both phenomena being highly dependent on target antigen (Ag) recognition. In solid tumours, target Ag recognition occurs exclusively in the tumour, but the low Ag levels, together with the immunosuppressive microenvironment, prevent the activation of CAR-T cells. We believe that promotion of CAR-T-cell activation through off-tumour recognition of the target Ag may substantially improve the efficacy of CAR-T therapy in solid tumours. This may be safely achieved using vaccines able to deliver the target Ag. To test our hypothesis, we chose a CAR tumour Ag with low surface density expression, such as gp75 expressed in B16 melanoma cells. We studied the role of a Semliki Forest virus (SFV)-based vaccine encoding a mutant gp75 protein (gp75mut), which exhibits enhanced surface expression. We demonstrate that SFVgp75mut vectors increased the activation and expansion of cognate CAR-T cells in vitro. In an immunocompetent mouse model, intratoumoral administration of SFVgp75mut vaccine strongly increased the number of gp75CAR-T cells within the tumour. More importantly, SFVgp75mut in combination with gp75CAR-T cells delayed tumour growth and enhanced overall survival. Interestingly, the combination also exerted antitumoral effect on distal, non-SFVgp75mut-treated tumours. Our data show SFV-based vaccines increase the efficacy of CAR-T therapy in solid tumours, with the local administration of these vaccines being able to exert abscopal effects.