Disruptions in the physiological functioning of these enzymes - either through mutations, their overexpression, or their abnormal activation is a characteristic hallmark of numerous cancers (e.g., BRAF in melanoma → leading to the constitutive activation of the MAP kinase pathway, HER2/ERBB2 overexpression in breast cancer, BCR-ABL fusion in chronic myeloid leukemia [CML] → leading to constitutive kinase activation), making PKs as attractive therapeutic targets for the development of novel anticancer drugs (Kannaiyan and Mahadevan, 2018[60]). The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.