In breast cancer, overexpression of miR-335 resulted in an increase in tumor suppressor gene BRCA1, leading to decreased cell viability and increased apoptosis.24 In small cell lung cancer, loss of miR-335 promoted metastatic skeletal lesions via deregulation of IGF-IR and RANKL pathways.25 On the contrary, the potential oncogenic role of miR-335 was identified by showing its elevated expression in malignant astrocytomas, gastric cancer recurrence samples, and pediatric AML.12,13,26–29. This evidence concerns the gene IGF1R and gastric cancer.