Although upregulation of endogenous ILK has been variously implicated as oncogenic or tumor-suppressive, the ILKR211A mutation, which is resistant to receptor-mediated activation[6] and to angiotensin II-induced cardiac hypertrophy induction[2], is also either phenotypically inert or growth suppressive in a broad range of cancer lines[7,13]. Here, ILK is linked to neoplasm.