This mutation is found in 90% of cases of WM/lymphoplasmacytic lymphoma, and the MYD88 L265P mutation is associated with a higher risk of disease progression but a better response to Bruton's tyrosine kinase inhibitors (BTKIs) therapy compared to others with wild-type MYD88. WM patients with CXCR4 mutations have decreased responses to BTKIs; in other words, responses to BTKIs are higher and deeper among those with mutated MYD88 and wild-type CXCR4 [10, 11]. This evidence concerns the gene CXCR4 and lymphoplasmacytic lymphoma.