Examples of such mechanisms were suggested by Mahendrarajah et al. [113] who attributed the synergy between MS-275 and dasatinib in the K-562 cell line to inactivation of p-ACK1 and p-STAT3, and by Chan et al. [114] who noted that thyroid cancer cell lines sensitive to dasatinib combinations with HDAC inhibitors carried mutations in the components of the MAPK pathway. The gene discussed is STAT3; the disease is thyroid gland carcinoma.