These same cells, when stimulated with IGF1, can decrease the expression of TIMP1. When PRKCZ is deregulated and over-expressed, it increases the translation or stability of IGF1R, thus enhancing IGF1 signalling, leading to a repression of ITGB3 expression, which ultimately can lead to changes in cellular processes that can enhance the aggressiveness of a tumour cell (eg. impaired apoptosis, increased proliferation). Here, ITGB3 is linked to neoplasm.