Because we hypothesized that fibroblasts could allocate CAV1-dependent apoptosis inhibiting proteins to the tumour cells, we investigated the presence and expression levels of well-known resistance-associated anti-apoptotic proteins in stromal HS5 fibroblasts being either proficient [HS5(+)] for CAV1 or CAV1-deficient [HS5(-)] achieved by a shRNA-mediated knock-down (Figure 1). This evidence concerns the gene CAV1 and neoplasm.